CENTRAL NERVOUS SYSTEM
EXCITATION IN THE CNS
151. THE PHENOMENON OF CHANGES IN THE NUMBER OF NERVE IMPULSES IN EFERENT FIBERS OF THE REFLECTOR ARC IN COMPARISON WITH AFFERENT FIBERS IS DUE TO
1) reflex aftereffect
3) post-tetanic potentiation
4) rhythm transformation in the nerve center
152. EXCITATION RHYTHM TRANSFORMATION
2) circulation of impulses in a neuron trap
3) random spread of excitation in the central nervous system
4) increase or decrease in the number of pulses
153. WITH INCREASING THE STRENGTH OF THE IRRITIVE, THE TIME OF THE REFLEX REACTION
1) does not change
2) increases
3) decreases
154. FATIGUE REFLEX TIME
1) does not change
2) decreases
3) increases
155. THE BASIS OF THE REFLECTOR CONSEQUENCE IS
1) spatial summation of impulses
2) transformation of impulses
3) sequential summation of pulses
4) circulation of impulses in a neuron trap
156. DIFFUSE IRRADIATION OF EXCITATION IS UNDERSTAND
2) change in the rhythm of excitation
3) slow spread of excitation through the central nervous system
4) non-directional spread of excitation through the central nervous system
157. INCREASING TRANSFORMATION OF THE RHYTHM OF EXCITATION IN THE NERVOUS SYSTEM IS DUE TO
1) dispersion of excitations and low lability of nerve centers
2) synaptic delay
3) fatigue of nerve centers and dispersion of excitations
4) dispersion and multiplication of excitations
158. THE ROLE OF CNS SYNAPSE IS THAT THEY
1) are the site of excitation in the central nervous system
2) form the resting potential of the nerve cell
3) conduct quiescent currents
4) transmit impulses from neuron to neuron
159. IN A REFLECTOR ARCH WITH THE LOWEST SPEED, EXCITATION IS PROPAGATED
1) afferent
2) efferent
3) central
160. REFLEX TIME
1) the end of the action of the stimulus
2) achieving a useful adaptive result
3) occurrence of a response
161. OCCLUSION IS BASED ON PROCESSES
1) prolongation
2) dispersion
3) animations
4) convergence
162. REFLEX TIME DEPENDS ABOVE ALL
1) from irradiation of excitation
2) from physical and chemical properties effector
3) on the physiological properties of the effector
4) on the strength of the stimulus and the functional state of the central nervous system
163. EXCITATION IN THE NERVE CENTER SPREADS
1) from the efferent neuron through the intermediate to the afferent
2) from intermediate neurons through the efferent neuron to the afferent
3) from intermediate neurons through an afferent neuron to an efferent one
4) from the afferent neuron through the intermediate to the efferent
164. THE ROLE OF THE REVERSE AFFERENTATION LINK IS TO PROVIDE
1) morphological connection of the nerve center with the effector
2) spread of excitation from the afferent link to the efferent
3) assessment of the result of the reflex act
165. NERVE CELL PERFORMS ALL FUNCTIONS EXCEPT
1) receiving information
2) information storage
3) encoding information
4) mediator production
5) mediator inactivation
166. THE MAIN FUNCTION OF DENDRITS IS
1) conduction of excitation from the cell body to the effector
2) mediator production
3) conduction of excitation to the body of the neuron
167. IN NATURAL CONDITIONS AN ACTION POTENTIAL IN A NEURON ARISES
1) in the area of dendrites
2) in the synapse
3) in the soma of the nerve cell
4) in the initial segment of the axon
168. CONDUCTION OF EXCITATION IN THE CNS
1) electrical
2) mixed
3) chemical
169. INTEGRATIVE ACTIVITY OF A NEURON CONSISTS IN
1) post-tetanic potentiation
2) connections with other neurons through processes
3) summation of all postsynaptic potentials arising on the neuron membrane
170. EXCITATIVE POSTSYNAPTIC POTENTIAL ARISES WITH LOCAL
1) hyperpolarization
2) depolarization
171. EXCITATIVE POSTSYNAPTIC POTENTIAL DEVELOPES AS A RESULT OF OPENING ON THE POSTSYNAPTIC MEMBRANE OF CHANNELS FOR IONS
3) sodium
172. EXCITATIVE POSTSYNAPTIC POTENTIAL IS A LOCAL PROCESS OF DEPOLARIZATION DEVELOPING ON THE MEMBRANE
1) axon hillock
2) sarcoplasmic
3) mitochondrial
4) presynaptic
5) postsynaptic
173. IMPULSES ARE GENERATED WITH A HIGHER FREQUENCY
4) 50 ms
174. A COMPLEX OF STRUCTURES NECESSARY FOR THE IMPLEMENTATION OF A REFLEX REACTION IS CALLED
1) functional system
2) nerve center
3) neuromuscular drug
4) dominant focus of excitation
5) reflex arc
175. AT PROLONGED IRRITATION OF THE SKIN OF A FROG'S LEGS THE REFLEX WITHDRAWAL OF THE FOOT IS STOPPED BECAUSE OF THE DEVELOPMENT OF FATIGUE
1) in the muscles of the paw
2) in neuromuscular synapses
3) in the nerve center of the reflex
176. INCREASE IN THE NUMBER OF EXCITED NEURONS IN THE CNS WHEN INCREASED IRRITATION IS DUE TO
1) spatial summation
2) relief
3) occlusion
4) irradiation
177. DISTRIBUTION OF EXCITATION FROM ONE AFFERENT NEURON TO MANY INTERNEURONS IS CALLED A PROCESS
1) rhythm transformation
2) spatial summation
3) relief
4) common final path
5) irradiation
178. ONE MOTONEURON CAN RECEIVE IMPULSES FROM SEVERAL AFFERENT NEURONS AS A RESULT OF
1) afferent synthesis
2) sequential summation
3) divergences
4) convergence
179. STRENGTHENING OF THE REFLECTOR REACTION CANNOT OCCUR AS A RESULT OF
1) inhibition of the antagonist reflex
2) post-tetanic potentiation
3) sequential summation
4) relief
5) occlusion
180. POST-TETANIC POTENTIAL CONSISTS IN STRENGTHENING THE REFLEX REACTION TO IRRITATION PREVIOUS
1) inhibition of the nerve center
2) spatial summation of impulses
3) step down transformation of impulses
4) rhythmic stimulation of the nerve center
181. SPATIAL SUMMATION OF PULSES IS PROVIDED
1) divergence of excitation
2) the presence of a dominant focus of excitation
3) the presence of feedback
4) excitation convergence
182. NOT CHARACTERISTIC FOR NEURONS OF DOMINANT FOCUS
1) the ability to sum up excitations
2) the ability to transform the rhythm
3) high lability
4) inertia
5) low lability
183. NERVE CENTERS DO NOT HAVE THE PROPERTIES
1) plasticity
2) high sensitivity to chemical irritants
3) the ability to sum up excitations
4) the ability to transform the rhythm
5) bilateral conduction of excitations
184. PLASTICITY OF SYNAPSE IS CHARACTERISTIC
1) only for motor neurons of the spinal cord
2) only for higher parts of the central nervous system
3) for any part of the CNS
185. PARTICIPATION IN DIFFERENT REFLECTOR REACTIONS OF THE SAME EFFERENT NEURONS AND EFFECTORS IS DUE TO THE PRESENCE
1) plasticity of nerve centers
2) polyfunctionality of neurons
3) divergence of excitations
4) breaking the path
5) common final path
186. EXCESS OF THE EFFECT OF THE SIMULTANEOUS ACTION OF TWO WEAK AFFERENT EXCITATIONS
OVER THE SUM OF THEIR SEPARATE EFFECTS ARE CALLED
1) summation
2) transformation
3) animation
4) irradiation
5) relief
187. WEAKER EFFECT OF SIMULTANEOUS ACTION OF TWO STRONG AFFERENT INPUTS TO THE CNS,
WHAT THE SUM OF THEIR SEPARATE EFFECTS IS CALLED
1) braking
2) down transformation
3) convergence
4) negative induction
5) occlusion
Set match.
THE PRINCIPLE OF COORDINATING ACTIVITY OF THE CNS .... CONSOLIDATES
A.2 Facilitation 1. In reducing the effect of simultaneous
B.1 Occlusion of the action of two strong stimuli
compared to the sum of their separate effects.
2. In excess of the effect of the simultaneous action of two weak stimuli over the sum of their separate effects.
THE PRINCIPLE OF COORDINATING ACTIVITY OF THE CNS .... CONSOLIDATES
A.1 Common final path 1. In participation in various reflex reactions
B. 2 The principle of dominance of the same efferent neurons and effectors.
2. There is a center in the brain that has increased excitability, inertia and the ability to slow down and summarize the excitations of other nerve centers.
THE PROPERTY OF THE NERVE CENTER .... IS MANIFESTED
A.2 Post-tetanic 1. In the ability to change one's
potentiation function, expand functionality
B.3 Low accommodative 2. Intensification of the reflex reaction after a long rhythmic ability to stimulate the nerve center.
3. In the ability to respond to stimuli that slowly increase in strength.
CNS CELLS .... PERFORM FUNCTIONS
A.3 Nervous 1. Absorption of excess neurotransmitter, formation of the myelin sheath, provision of trophism.
B.1 Glial 2. Perception of stimulus energy and its transformation into a nerve impulse.
3. Reception, processing, storage and transmission of information.
CHANGES IN THE REFLECTOR REACTION .... ARE DUE TO
A.2 Slowdown 1. Posttetanic potentiation.
B.1 Strengthening 2. Fatigue of the nerve center.
3. Circulation of impulses in a neuron trap.
A.2 Reduction of time 1. Circulation of impulses in a neuron trap.
reflex 2. Increasing the strength of irritation.
B.3 Weakening of response 3. Occlusions.
CHANGES IN THE REFLECTOR REACTION .... ARE DUE TO
A.3 Strengthening the reflex 1. Inhibition of the nerve center.
answer 2. Circulation of impulses in a neuron trap
B.2 Reflex aftereffect 3. Relief.
CHANGES IN THE REFLECTOR REACTION .... ARE DUE TO
A.1 Slowdown 1. Fatigue of the nerve center.
B.2 Reducing time 2. Increasing the strength of irritation.
reflex 3. Occlusion.
A PHENOMENON THAT OCCURS IN THE CNS.... IS DUE TO
A.1 Occlusion 1. Convergence of excitations.
B.4 Downward transformation - 2. Circulation of impulses in the neuron
rhythm excitation trap.
B.3 Increasing transformation - 3. Dispersion and irradiation of excitation.
mation of rhythms of excitations 4. Summation of EPSP.
EXAMPLE OF REFLEX .... REACTION
A.1 Is 1. The contraction of the muscles of the intestine when a portion of chyme enters
B.2 Not 2. Contraction of the intestinal muscles after the application of acetylcholine.
EXAMPLE OF REFLEX .... REACTION
A.1 Is 1. Constriction of the pupil with a bright flash of light.
B.2 Not 2. Pupil dilatation when atropine (a cholinergic receptor blocker) is instilled into the eye.
REFLECTOR ARC LINK....PERFORMS FUNCTIONS
A.4 Receptor 1. Transmits information about the work of the effector to the cerebral cortex
B.3 Afferent 2. Centrifugal conduction of excitation from the nerve center to the effector structure
B.5 Central 3. Centripetal conduction of excitation from receptors to the nerve center.
D.2 Efferent 4. Perceives the energy of the stimulus and converts it into a nerve impulse.
5. Performs analysis and synthesis of the received information.
200. Excitation in a neuron occurs first of all in the region of the soma, because only excitatory postsynaptic potentials are summed on the membrane of the body of the neuron.
5) HHH
201. If the motor neurons of the spinal cord are damaged, the skeletal muscles of the limbs lose their ability to contract, because the muscles are innervated by the dendrites of the motor neurons.
5) VNN
202. In case of damage to the motor neurons of the spinal cord, the skeletal muscles of the limbs lose their ability to contract, because the muscles are innervated by the axons of the motor neurons.
5) VVV
203. A frog with a destroyed spinal cord lacks all spinal reflexes, because reflex acts begin with excitation of the nerve center.
5) VNN
204. The knee reflex is referred to as polysynaptic, because in the reflex arc of the knee reflex
there is one central and many neuromuscular synapses.
5) NVN
205. The knee reflex is classified as monosynaptic, because there is only one central synapse in the structure of the knee reflex.
5) VVV
206. In a reflex arc, excitation is always conducted in only one direction, because the synapses
transmitting excitation from afferent to efferent neurons, have one-way conduction of impulses.
5) VVV
207. In a reflex arc, excitation can be carried out in the forward and reverse directions, because the structure of the reflex has a link of reverse afferentation.
5) NVN
208. When the anterior roots of one segment of the spinal cord are damaged, the sensitivity in the corresponding metamere of the body does not completely disappear, but only weakens, because each anterior root of the spinal cord innervates three metameres of the body - its own and two adjacent to it.
5) NVN
209. When the anterior roots of one segment of the spinal cord are damaged, the motor activity in the corresponding metamere of the body only weakens, but does not stop completely, because each metamere is innervated from three neighboring segments of the spinal cord.
5) VVV
210. If one segment of the spinal cord is damaged, motor activity in the corresponding metamere of the body stops, because motor neurons of skeletal muscles are localized in the spinal cord.
5) NVN
211. When the posterior roots of one segment of the spinal cord are affected, sensitivity in the corresponding metamere of the body disappears, because the posterior roots of the spinal cord consist of afferent nerve fibers.
5) NVN
INHIBITION IN THE CNS
Choose one correct answer.
212. EVERYTHING IS REQUIRED FOR THE DEVELOPMENT OF INHIBITION IN THE CNS, EXCEPT
1) mediator
2) ATP energy
3) opening of chloride channels
4) opening of potassium channels
5) violations of the integrity of the nerve center
213. THE MEDIATOR OF THE INDUSTRIAL NEURON, AS A RULE, ON THE POSTSYNAPTIC MEMBRANE, CAUSES
1) static polarization
2) depolarization
3) hyperpolarization
214. REFLEX TIME IN SECHENOV'S EXPERIENCE
1) does not change
2) is not determined in this experiment
3) decreases
4) increases
215. IN SECHENOV'S EXPERIENCE
1) breast and lumbar regions spinal cord
2) medulla oblongata and spinal cord
3) between visual tubercles and overlying departments
216. INHIBITION WAS DISCOVERED BY SECCHENOV AT IRRITATION
1) spinal cord
2) medulla oblongata
3) cerebral cortex
4) cerebellum
5) thalamus
217. DURING THE DEVELOPMENT OF PESSIMAL INHIBITION, THE NEURON MEMBRANE IS IN THE STATE
1) static polarization
2) hyperpolarization
3) sustained prolonged depolarization
218. THE PHENOMENON IN WHICH EXCITATION OF ONE MUSCLE IS ACCOMPANIED BY INHIBITION OF THE CENTER OF THE ANTAGONIST MUSCLE IS CALLED
1) negative induction
2) occlusion
3) relief
4) fatigue
5) reciprocal inhibition
219. BRAKING IS A PROCESS
1) always spreading
2) propagating if IPSP reaches a critical level
3) local
220. SPECIFIC BRAKE NEURONS ARE
1) neurons of the substantia nigra and the red nucleus of the midbrain
2) pyramidal cells of the cerebral cortex
3) neurons of the Deiters nucleus of the medulla oblongata
4) Purkinje and Renshaw cells
221. THE PHENOMENON OF CONNECTED DECELERATION CAN BE OBSERVED
1) in Sechenov's experiment
2) with simultaneous stimulation of the receptive fields of two spinal reflexes
3) in an experiment when, during the development of one reflex, the receptive field of an antagonistic reflex is irritated
222. THE SIGNIFICANCE OF RECIPROCAL INHIBITION IS
1) in the performance of a protective function
2) in the release of the central nervous system from the processing of non-essential information
3) in ensuring the coordination of the work of antagonist centers
223. IPSP DUE TO CHANGES IN THE PERMEABILITY OF THE MEMBRANE FOR IONS
2) sodium and chlorine
3) potassium and chlorine
224. THE APPEARANCE OF PESSIMAL BRAKING IS PROBABLY
1) at low pulse frequency
2) with the secretion of inhibitory mediators
3) upon excitation of intercalary inhibitory neurons
4) with increasing pulse frequency
225. PRESYNAPTIC INHIBITION IS IMPLEMENTED THROUGH SYNAPSES
1) axo-somatic
2) somato-somatic
3) axo-dendritic
4) axo-axonal
226. THE MECHANISM OF PRESYNAPTIC INHIBITION IS RELATED
1) with hyperpolarization
2) with the operation of the K - Na pump
3) with CA pump operation
4) with prolonged depolarization
227. FROM THE POINT OF VIEW OF THE BINARY-CHEMICAL THEORY, THE PROCESS OF BRAKING ARISES
3) in the same structures and with the help of the same mediators as the excitation process
4) during the functioning of special inhibitory neurons that produce special mediators
228. FROM THE POINT OF VIEW OF THE UNITARY-CHEMICAL THEORY, BRAKING APPEARS
1) due to inactivation of cholinesterase
2) with a decrease in the synthesis of the excitatory mediator
3) during the functioning of special inhibitory neurons that produce special mediators
4) in the same structures and with the help of the same mediators as the excitation process
229. THE PHENOMENON OF PESSIMAL BRAKING WAS DISCOVERED
1) Ch. Sherrington
2) I.M. Sechenov
3) I.P. Pavlov
4) the Weber brothers
5) NOT. Vvedensky
230. THE PHENOMENON OF CENTRAL BRAKING WAS DISCOVERED
1) the Weber brothers
2) Ch. Sherrington
3) I.P. Pavlov
4) I.M. Sechenov
231. BRAKING IS A PROCESS
1) arising from the fatigue of nerve cells
2) leading to a decrease in the KUD of the nerve cell
3) arising in receptors with excessively strong stimuli
4) preventing the occurrence of excitation or weakening the excitation that has already arisen
232. BRAKING IS REQUIRED IN THE WORK OF THE NERVE CENTERS
1) to close the arc of reflexes in response to irritation
2) to protect neurons from excessive excitation
3) to combine CNS cells into nerve centers
4) to ensure the safety, regulation and coordination of functions
233. DIFFUSIVE IRRADIATION CAN BE STOP AS A RESULT OF
1) the introduction of strychnine
2) increase the strength of the stimulus
3) lateral inhibition
234. THE DEVELOPMENT OF INDERATION IN SECHENOV'S EXPERIMENT ON A FROG IS JUDGED BY
1) the appearance of convulsive contractions of the legs
2) decrease in heart rate followed by cardiac arrest
3) change in spinal reflex time
235. CONTRACTION OF THE FLEXOR MUSCLES WITH SIMULTANEOUS RELAXATION OF THE EXTENSOR MUSCLES IS POSSIBLE AS A RESULT OF
1) outdoor activities
2) relief
3) negative induction
4) pessimal inhibition
5) reciprocal inhibition
236. INHIBITION OF NEURONS BY OWN IMPULSES COMING THROUGH AXON COLLATERALS
TO THE BRAKE CELLS, REFERRED
1) secondary
2) reciprocal
3) progressive
4) lateral
5) returnable
237. WITH THE HELP OF RENSHOW'S BRAKING INTERCHANGE CELLS BRAKING IS CARRIED OUT
1) reciprocal
2) lateral
3) primary
4) returnable
238. INHIBITION OF MOTONEURONS OF ANTAGONIST MUSCLES DURING LIMB FLEXION AND EXTENSION IS CALLED
1) progressive
2) lateral
3) returnable
4) reciprocal
239. WHEN THE LIMB flexes, the intercalary inhibitory neurons of the extensor muscle center should be
1) at rest
2) are inhibited
3) excited
240. BRAKING EFFECT OF A SYNAPSE LOCATED NEAR THE AXON COLLECTION
COMPARED WITH OTHER PARTS OF THE NEURON MORE
2) strong
241. DEVELOPMENT OF INHIBITION OF NEURONS PROMOTES
1) depolarization of the membrane of the axon hillock and the initial segment
2) depolarization of the soma and dendrites
3) hyperpolarization of the axon colliculus membrane
242. BY ITS MECHANISM, POSTSYNAPTIC INHIBITION CAN BE
1) only depolarizing
3) and de- and hyperpolarizing
243. BY ITS MECHANISM, PRESYNAPTIC INHIBITION CAN BE
1) both de- and hyperpolarization
2) only hyperpolarization
3) only depolarizing
Set a match.
DURING BRAKING..... ON THE SUBSYNAPTIC MEMBRANE
A.2 Presynaptic 1. Short-term depolarization.
B.3 Postsynaptic 2. Prolonged depolarization.
3. Hyperpolarization or prolonged depolarization.
THEORIES OF BRAKING .... ARE THAT
A.3 Unitary-chemical 1. Braking is a consequence of fatigue.
B.2 Binary-chemical 2. Inhibition occurs as a result of the functioning of inhibitory neurons.
3. Inhibition manifests itself in the same structures and with the help of the same mediators as excitation.
NERVOUS PROCESS .... CHARACTERIZE SIGNS
A.2 Excitation 1. Always a local process that manifests itself
B.1 Inhibition in long-term stable depolarization or hyperpolarization of the neuron membrane.
2. Local or spreading process due to the opening of sodium channels.
PHENOMENON.... DEVELOPING AS A RESULT OF
A.4 Pessimal 1. Continuous DC
deceleration in the area of application of the cathode.
B.1 Cathodic 2. Short-term action of direct current in the area of application of the cathode.
depression 3. Irritation of the vagus nerve.
4. Increasing the frequency of impulses.
5. Simultaneous stimulation of the receptive fields of two spinal reflexes.
RESEARCHERS .... CNS PHYSIOLOGY MADE THE FOLLOWING CONTRIBUTION TO THE DEVELOPMENT
A.2 A.A. Ukhtomsky 1. Formulated the principles of general
B.3 Berger of the final path and reciprocity.
B.1 Ch. Sherrington 2. Developed the doctrine of the dominant.
3. First recorded EEG in humans.
BRAKING .... REACTION
A.2 Is 1. Disappearance of the patellar reflex in case of trauma to the lumbar spine.
B.1 Is not 2. Cessation of salivation in the process of eating when there is severe pain in the abdomen.
TYPE OF BRAKING....PERFORMS A FUNCTION
A.2 Lateral 1. Suppresses the excitation of the center
B.4 Recurrent antagonistic function.
B.1 Reciprocal 2. Eliminates diffuse irradiation of excitation.
3. Stops the release of the mediator into the synaptic cleft.
4. Weakens the excitation of motor neurons by their own impulses through Renshaw cells.
TYPES OF NEURONS ... ARE
A.3 Alpha motor neuron 1. Neuron of the motor zone of the cerebral cortex.
B.2 Gamma motor neuron 2. Neuron of the anterior horns of the spinal cord,
B.1 Giant pyra - midal skeletal muscle cell innervating intrafusal fibers.
Betsa 3. Neuron of the anterior horns of the spinal cord,
D.5 Renshaw cell innervating extrafusal fibers of skeletal muscles.
4. Inhibitory neuron of the cerebellar cortex.
5. Inhibitory interneuron of the spinal cord.
TYPES OF POSTSYNAPTIC POTENTIALS OF A NEURON ..... ARE DUE TO THE OPENING OF CHANNELS FOR IONS
A.1 EPSP 1. Sodium.
B.23 TPSP 2. Potassium.
4. Calcium.
AT ACTIVATION OF CHLORINE CHANNELS... THE CURRENT OF CHLORINE IONS IS OBSERVED...
A.1 Presynaptic 1. Out of the cell.
B.2 Postsynaptic 2. From the external environment into the cell.
Determine whether the statements are true or false and the relationship between them.
254. Inhibition of the spinal reflex in Sechenov's experiment is caused by irritation of the visual tubercles with a crystal of sodium chloride, because sodium and chloride ions cause hyperpolarization of neurons.
5) VNN
255. Presynaptic inhibition is very effective in processing information coming to the neuron, because during presynaptic inhibition, excitation can be selectively suppressed at one synaptic input without affecting other synaptic inputs.
5) VVV
256. To demonstrate the role of inhibition, strychnine is injected into a frog, because strychnine activates inhibitory synapses.
5) VNN
257. To demonstrate the role of inhibition, strychnine is injected into a frog, because strychnine blocks inhibitory synapses.
5) VVV
258. To demonstrate the role of inhibition, strychnine is injected into a frog, because after the administration of strychnine, the frog exhibits
diffuse irradiation of excitation.
5) VVV
259. A neuron can be in a state of rest, excitation or inhibition, because on one neuron they can be summed up
either excitatory or inhibitory postsynaptic potentials.
5) VNN
260. Only EPSP or only TPSP can be summed on one neuron, because according to the Dale principle, one neuron uses
in all their terminals there is only one type of mediator.
5) NVN
261. Either excitation or inhibition can spread along the axon of a neuron, because during the summation of EPSP
and IPSP total potential can be either positive or negative.
5) NVN
262. Sechenov's experiment is carried out on a spinal frog, because the time of the spinal reflex is measured in Sechenov's experiment.
5) NVN
263. Sechenov's experiment is carried out on a thalamic frog, because for the manifestation of the spinal reflex in Sechenov's experiment, it is necessary to place a salt crystal on the visual tubercles.
5) VNN
MUSCLE TONE
Choose one correct answer.
264. MUSCLE TONE AFTER TRANSACTION
1) will not change much
2) disappear
3) extensor tone will increase
4) will decrease significantly
265. CONTRACTILLE TONE IN TRANSACTION OF THE POSTERIOR ROOTS OF THE SPINAL CORD
1) will not change much
2) extensor tone will increase
3) will decrease significantly
4) disappear
266. IN TRANSACTION
1) will not change much
2) disappear
3) will decrease significantly
4) extensor tone will be higher than the flexor tone
267. MUSCLE TONE IN TRANSACTION OF THE ANTERIOR ROOTS OF THE SPINAL CORD
1) will not change much
2) extensors will increase
3) will decrease significantly
4) disappear
268. THE INFLUENCE OF THE RED NUCLEAR ON THE NUCLEAR OF THE DUTARSA IS
1) exciting
2) insignificant
3) brake
269. BLACK SUBSTANCE ON RED NUCLEUS INFLUENCES
1) exciting
2) very weak
3) brake
270. INTRAFUSAL MUSCLE FIBERS ARE INNERVATED BY MOTONEURONS
3) gamma
271. EXTRAFUSAL MUSCLE FIBERS ARE INNERVATED BY MOTONEURONS
3) alpha
272. INTRAFUSAL MUSCLE FIBERS PERFORM THE FUNCTION
1) muscle contractions
2) muscle relaxation
3) ensuring the sensitivity of the Golgi apparatus to stretching
4) ensuring the sensitivity of the "muscle spindle" to stretching
273. EXTRAFUSAL MUSCLE FIBERS PERFORM THE FUNCTION
1) ensuring the sensitivity of the "muscle spindle" to stretching
2) ensuring the sensitivity of the Golgi apparatus to stretching
3) contractions of the "muscle spindle"
4) muscle contraction
274. THE BODIES OF ALPHA-MOTONEURONS ARE LOCATED IN THE HORN OF THE SPINAL CORD
2) side
3) front
275. GAMMA-MOTONEURON BODIES ARE LOCATED IN THE HORN OF THE SPINAL CORD
2) side
3) front
276. MUSCLE TONE APPEARS AT TRANSACTION
1) normal
2) plastic
3) spinal
4) contractile
277. IF THE CONNECTION BETWEEN THE BASAL GANGLIA AND THE MIDDLE BRAIN IS DISTURBED,
THAT IS MUSCLE TONE
1) normal
2) contractile
3) spinal
4) plastic
278. EXCITATION PULSES TO THE NUCLEAR OF DUTERS
1) from proprioceptors
2) from the midbrain
3) from the cerebral cortex
4) from vestibular analyzer receptors
279. GOLGI APPARATUS IS LOCATED
2) in the distal parts of intrafusal fibers
3) among extrafusal muscle fibers
4) in muscle tendons
280. SENSITIVE TERMINATIONS OF THE PRIMARY AFFERENTS OF THE MUSCLE SPINDLE ARE
1) in the distal itrafusal fibers
3) in the tendons of the muscle
4) in the nuclear bag of intrafusal fibers
281. SENSITIVE ENDINGS OF THE SECONDARY AFERENTS OF THE MUSCLE SPINDLE ARE
1) in the nuclear bag of intrafusal fibers
2) among extrafusal muscle fibers
3) in the tendons of the muscle
4) in the distal intrafusal fibers
282. FAST (PHASE) MOVEMENT IS PROVIDED BY MUSCLE FIBERS
1) intrafusal
2) red
3) white
283. SLOW TONIC MOVEMENT IS PROVIDED BY MUSCLE FIBERS
1) intrafusal
3) red
284. MUSCLE FIBERS PARTICIPATE IN RECEPTION OF MUSCLE STATE
2) red
3) intrafusal
285. EXCITATION OF GAMMA-MOTONEURONS WILL LEAD
4) to contraction of intrafusal muscle fibers
286. EXCITATION OF GOLGI RECEPTORS WILL LEAD
1) to the reduction of white muscle fibers
2) to the contraction of extrafusal muscle fibers
3) to contraction of intrafusal muscle fibers
4) to relax extrafusal muscle fibers
287. EXCITATION OF THE ALPHA MOTOR NEURON WILL LEAD
1) to reduce all muscle fibers
2) to contraction of intrafusal muscle fibers
3) to relaxation of extrafusal muscle fibers
4) contraction of extrafusal muscle fibers
288. REFLEXES THAT APPEAR TO MAINTAIN POSES DURING MOVEMENT ARE CALLED
1) static
2) kinetic
3) somatic
4) statokinetic
289. WEAK MUSCLE TONE IS OBSERVED IN THE EXPERIMENT IN AN ANIMAL
1) diencephalic
2) thalamic
3) mesencephalic
4) bulbar
5) spinal
290. THE STRONGEST MUSCLE TONE IS EXPERIENCED IN AN ANIMAL
1) intact (all parts of the central nervous system are preserved)
2) diencephalic
3) thalamic
4) mesencephalic
5) bulbar
291. NOT OBSERVED IN CERENERLAL INSUFFICIENCY
1) impaired coordination of movements
2) violation of the knee jerk
3) change in muscle tone
4) vegetative disorders
5) loss of consciousness
292. NOT CHARACTERISTIC FOR ANIMALS WITH DECEREBRATIVE RIGIDITY
1) change of normal posture
2) the disappearance of rectifying reflections
3) disappearance of the lift reflex
4) a sharp increase in the tone of the extensor muscles
5) a sharp decrease in the tone of the extensor muscles
293. IN THE SPINAL CORD THE ARCHES OF ALL THE LISTED REFLEXES ARE CLOSED, EXCEPT
2) plantar
3) urinary
4) flexion
5) rectifier
Set a match.
TYPES OF NERVE FIBERS ... HAVE FUNCTIONAL FEATURES
A.3 A-alpha 1. Postganglionic autonomic fibers and afferent fibers from heat receptors,
B.4 A-gamma of pressure and pain, having the lowest speed of excitation (0.5-3 m / s)
B.2 B 2. Preganglionic vegetative fibers having a speed of excitation 3-10 m/sec.
D.1 C 3. Axons of motor neurons innervating skeletal muscles, and afferent fibers from muscle receptors, which have the highest speed of excitation conduction - up to 120 m / s.
4. Afferent fibers from touch and pressure receptors and efferent fibers to muscle spindles, having an excitation conduction speed of 15-40 m/s
5. Afferent fibers from some receptors of heat, pressure and pain, having a speed of excitation conduction of 5-15 m / s.
NEURONS .... PERFORM FUNCTIONS
A.2 Motor neuron 1. Participates in the formation of the corticospinal, cortico-bulbar tracts.
B.1 Giant pyramidal 2. Causes contraction of skeletal muscle fibers.
Betz cell 3. Inhibits the activity of the nuclei of the medulla oblongata.
B.4 Renshaw cell 4. Provides recurrent inhibition of motor neurons of the spinal cord.
MOTONERONS .... PERFORM FUNCTIONS
A.3 Alpha-1. They transmit information about the stretching of the extrafusal fibers of skeletal muscles to the CNS.
B.2 Gamma-2. Causes contraction of intrafusal skeletal muscle fibers.
3. Causes contraction of extrafusal skeletal muscle fibers.
4. Causes relaxation of extrafusal fibers of skeletal muscles.
IN THE DEPARTMENT OF THE CNS ... ARE LOCATED
A.2 Medulla oblongata 1. Speech center.
B.4 Midbrain 2. Centers - vasomotor, respiratory, chewing, salivation, swallowing.
B.5 Thalamus 3. Higher subcortical centers of the autonomic nervous system.
D.3 Hypothalamus 4. Centers for the regulation of muscle tone and involuntary coordination of movement.
5. Centers for the integration of sensory information from extra- and interoreceptors during transmission to the cerebral cortex.
TONIC REFLEXES .... APPEAR WHEN
A.3 Postures (positions) 1. The action of visual and auditory signals.
B.2 Rectifying 2. Violation of the natural posture.
B.4 Statokinetic 3. Excitation of vestibular receptors when the position of the head changes.
4. Excitation of vestibular receptors when the speed of body movement changes.
REFLEXES .... HAVE ADAPTABLE RESULT IN THE FORM
A.2 Posnotonic 1. Maintaining posture when changing
B.3 Rectifying 2. Prevention of imbalance when changing the position of the head.
B.1 Statokinetic 3. Restoring the natural posture when it changes.
4. Turning the head to a visual or auditory signal for better perception of information.
REFLEX .... CLOSE AT THE CNS LEVEL
B.3 Plantar 2. Bulbarnoe.
B.1 Lift 3. Spinal.
D.1 Rectifier 4. Thalamic.
E.2 Swallowing
IMPACT..... LEADS TO EFFECT
A.2 Simultaneous stimulation 1. Manege movements of the animal,
two receptive fields weakening muscle tone by
(skin of two hind legs on one side of the body.
B.2 Simultaneous irritation 2. Prolongation of spinal
thalamus and skin posterior flexor reflex.
frog legs 3. Gradual involvement in the reflex
B.3 Irritation of the posterior skin by the muscles of the intact legs.
frog legs single
PHYSIOLOGICAL EXPERIMENT... LEADS TO EFFECT
A.5 Consistent violation 1. Change in the strength of muscle tone,
anatomical or physiological posture and motor activity.
physical integrity of structures 2. Manege movements of the animal,
reflex arc of the spinal weakening of muscle tone on
motor reflex in the frog to one side of the body.
B.1 Sequential transection 3. Prolongation of spinal
brain, starting with the flexion reflex.
higher departments, in experiment 4. Gradual involvement in the reflection
on an animal, the torsion response of the muscles of the second
B.3 Simultaneous irritation of the hind and both front paws
two receptive fields (frog skin.
two hind legs of a frog) 5. The absence of a reflex reaction.
D.3 Simultaneous irritation
thalamus and posterior skin
frog legs
E.4 Irritation of the posterior skin
frog legs single
growing strength stimuli
REFLEX .... APPEARS
A.1 Viscero- 1. In changing the activities of internal
visceral organs when irritated by their intero-
B.3 Visceroreceptors.
dermal 2. In changing the activity of internal organs
B.2 Somato- with irritation of certain
visceral areas of the skin.
3. In the change in sweating and skin sensitivity with irritation of the internal organs.
4. In the decrease in heart rate when pressing on the eyeballs.
5. In the inhibition of inspiration during stretching of the lungs.
TYPE OF TONE ... MANIFESTED IN THE ANIMAL
A.4 Uniform, but 1. Intact (all parts of the CNS are preserved).
Weakened 2. Thalamic.
B.3 Contractile 3. Bulbar.
B.2 Plastic 4. Spinal.
D.1 Normal
cerebellar insufficiency .... APPEARS
A.4 Asthenia 1. In violation of gait.
B.2 Astasia 2. In muscle tremor.
B.1 Ataxia 3. In the weakening of muscle tone.
4. In weakness and rapid muscle fatigue.
Determine whether the statements are true or false and the relationship between them.
306. The rectifying tonic reflex belongs to the group of stato-kinetic reflexes, because in order to restore the normal position of the body in violation of the posture, it is necessary to perform certain motor acts.
5) NVN
307. The lift reflex belongs to the group of stato-kinetic tonic reflexes, because the lift reflex occurs during acceleration rectilinear motion bodies in the vertical direction.
5) VVV
308. If the sacral spine is damaged, the knee reflex disappears, because the nerve center of the knee reflex is located in 1-2 segments of the sacral spinal cord.
5) HHH
309. The defeat of the pyramidal path leads to paralysis of the arms and legs, because the center of the motor reflexes of the upper and lower extremities is located in the pyramidal cells of the cerebral cortex.
5) VNN
310. When the tendon of the quadriceps femoris muscle is damaged, the Achilles reflex does not appear, because the Achilles reflex
related to tendon reflexes.
5) NVN
311. The knee reflex belongs to the group of static-kinetic tonic reflexes, because when the hammer strikes the tendon of the quadriceps femoris muscle, a sharp movement of the leg (extension of the lower leg) is observed.
5) NVN
312. The Achilles reflex belongs to the group of tonic reflexes, because when the foot is flexed during this reflex, the
tone of the flexor and extensor muscles.
5) NVN
313. The medulla oblongata is involved in the regulation of muscle tone, because the reticular formation and the vestibular nuclei of Deiters activate the motor neurons of the extensor muscles.
5) VVV
314. The midbrain is involved in the regulation of muscle tone, because the red nucleus of the midbrain activates the Deiters nucleus of the medulla oblongata.
5) VNN
315. Reflex spasm of the blood vessels of a limb is an example of a tonic reflex, because tonic reflexes are expressed in a change in the tone of the skeletal muscles.
5) NVN
AUTONOMIC SYSTEM
Choose one correct answer.
316. THE MEDIATOR OF THE PREGANGLIONARY FIBERS OF THE SYMPATIC NERVOUS SYSTEM
2) norepinephrine
3) serotonin
4) acetylcholine
317. THE MEDIATOR OF PREGANGLIONARY FIBERS OF THE PARASYMPATIC NERVOUS SYSTEM
2) norepinephrine
3) serotonin
4) acetylcholine
318. THE MEDIATOR OF POSTGANGLIONARY FIBERS OF THE SYMPATIC NERVOUS SYSTEM IS
1) acetylcholine
2) norepinephrine, adrenaline
3) serotonin
4) norepinephrine
319. THE MEDIATOR OF THE POSTGANGLIONARY FIBERS OF THE PARASYMPATIC NERVOUS SYSTEM IS
2) norepinephrine
3) serotonin
4) acetylcholine
320. THE SIMPLE VEGETATIVE REFLEX IS
1) monosynaptic
2) polysynaptic
321. PREGANGLIONARY FIBERS OF THE AUTONOMIC NERVOUS SYSTEM BELONG TO THE TYPE
322. POSTGANGLIONARY FIBERS OF THE AUTONOMIC NERVOUS SYSTEM BELONG TO THE TYPE
323. THE BODIES OF THE PREGANGLIONARY NEURONS OF THE SYMPATIC NERVOUS SYSTEM ARE LOCATED
1) in the posterior horns of the sacral segments of the spinal cord
2) in the lateral horns of the sacral segments of the spinal cord
3) in the posterior horns of the cervical and thoracic segments of the spinal cord
4) in the lateral horns of the cervical and thoracic segments of the spinal cord
324. THE BODIES OF THE PREGANGLIONARY NEURONS OF THE PARASYMPATIC NERVOUS SYSTEM ARE LOCATED
1) in the posterior horns of the sacral segments of the spinal cord, nuclei of the medulla oblongata
2) in the posterior horns of the cervical and thoracic segments of the spinal cord
3) in the lateral horns of the cervical and thoracic segments of the spinal cord
4) in the lateral horns of the sacral segments of the spinal cord, nuclei of the medulla oblongata and midbrain
325. INTERNEURONS OF THE METASYMPATHY NERVOUS SYSTEM ARE LOCATED
4) in the intramural ganglia
326. EFFERENT NEURONS OF THE METASYMPATHY NERVOUS SYSTEM ARE LOCATED
1) in the lateral horns of the spinal cord
2) in the posterior horns of the spinal cord
3) in the prevertebral ganglia
4) in the intramural ganglia
327. METASYMPATHY SYSTEM PROVIDES REGULATION
1) central
2) intercellular
3) intraorganic
328. THE HIGHEST CENTERS OF THE REGULATION OF VEGETATING FUNCTIONS ARE LOCATED
1) in the cerebral cortex
2) in the thalamus
3) in the medulla oblongata
4) in the hypothalamus
329. CORK OF THE HEMISPHERES ON THE ACTIVITY OF THE AUTONOMIC NERVOUS SYSTEM
1) does not affect
2) affects
Set a match.
VEGETATIVE REFLEXES .... OCCUR ON IRRITATION
A.1 Exteroceptive 1. Sensory receptors.
B.4 Viscero-visceral 2. Proprioreceptors.
B.2 Motor-visceral 3. Chemoreceptors of the hypothalamus.
4. Receptors of internal organs.
EFFERENT NEURONS OF THE DEPARTMENT OF THE AUTONOMIC SYSTEM..... INNERVATE
A.135 Sympathetic 1. Smooth muscles of the gastrointestinal tract.
B.15 Parasympathetic 2. Skeletal muscle fibers.
B.135 Metasympathetic 3. Smooth muscles of arterioles.
4. Neurons of the brain.
5. Secretory glands of the stomach.
THE EFFECTOR LINK OF THE REFLEX... COULD BE
A.23 Vegetative 1. Skeletal muscles.
B.1 Somatic 2. Smooth muscles.
3. Secretory glands of the digestive system.
4. Epithelial cells of the skin.
EFFERENT NEURONS .... ARE LOCATED
A. Sympathetic department of the CNS 1. In the intramural ganglia of the internal
B. Parasympathetic organs.
CNS 2. In the nuclei of the thalamus and hypothalamus.
3. In the ganglia of the sympathetic trunk.
DEPARTMENT OF THE AUTONOMOUS NERVOUS SYSTEM .... HAS MORPHOLOGICAL SIGNS
A.4 Sympathetic 1. Efferent neurons are always located only in the intramural ganglia and innervate only those internal organs that have their own motor rhythm (heart, intestines, uterus, gallbladder, etc.).
B.3 Parasympathetic 2. The efferent pathway can be represented
B.1 Metasympathetic cortico-, rubro-, vestibulo-, reticulospinal tract or axon of a motor neuron of the spinal cord.
3. The efferent path includes two neurons, while the axon of the first (preganglionic) is longer than the second.
4. The efferent pathway includes two neurons, of which the first is located in the thoracic or lumbar segments of the spinal cord, and the second is in the pre- or paraventebral ganglia.
DEPARTMENT OF THE AUTONOMOUS NERVOUS SYSTEM .... PERFORMS FUNCTIONS
A.1 Sympathetic 1. Activates the activity of the brain, mobilizes the protective and energy resources of the body; nerve fibers innervate all organs and tissues, including the cells of the nervous system.
B.3 Parasympathetic 2. Provides perception of external stimuli and contraction of skeletal muscles; nerve fibers are represented by type A.
B.4 Metasympathetic 3. Ensures the preservation of homeostasis by excitation or inhibition of the organs regulated by it; nerve fibers do not innervate skeletal muscles, the uterus, the central nervous system, and most of the blood vessels.
4. Provides homeostasis and control of the work of internal organs through structures located in the nerve nodes of the organs themselves.
Determine whether the statements are true or false and the relationship between them.
336. Trauma and diseases of the spine lead to dysfunction of the genitourinary system, secretion and motility of the digestive tract, blood pressure, because the centers of the spinal cord are involved in the regulation of many autonomic functions.
5) VVV
337. The efferent parasympathetic pathway has a two-neuron structure, because the centers of the parasympathetic division of the autonomic nervous system are localized in the brain and spinal cord.
5) VVN
338. The efferent sympathetic path has a two-neuron structure, because the centers of the sympathetic division of the autonomic nervous system are localized in the brain and spinal cord.
5) VNN
339. Preganglionic sympathetic fibers are shorter than postganglionic ones, because preganglionic sympathetic nerve fibers are of type B, and postganglionic are of type C.
5) VVN
340. Preganglionic sympathetic fibers are longer than postganglionic ones, because the preganglionic nerve fibers of the sympathetic division of the autonomic nervous system are of type B.
5) NVN
341. Intramural efferent neurons of the heart represent a common final path for the parasympathetic and metasympathetic divisions of the autonomic nervous system, because the intramural efferent neurons of the heart transmit excitation from both the preganglionic fibers of the vagus nerve and from the intramural intercalary neurons.
5) VVV
342. Many functions of the internal organs (for example, motor) are preserved after the transection of the sympathetic and parasympathetic pathways, because in the walls of these organs there is a metasympathetic system, including neurons-generators.
5) VVV
343. Metasympathetic nervous system regulates visceral organs faster than sympathetic and parasympathetic, because metasympathetic reflexes are local peripheral.
5) VVV
344. Metasympathetic mechanisms of regulation free the CNS from redundant information, because metasympathetic reflexes are closed outside the CNS - in the intramural ganglia.
5) VVV
345. The object of innervation of the sympathetic division of the autonomic nervous system is the whole organism, because sympathetic nerve fibers form plexuses around all vessels that bring blood to organs and tissues.
5) VVN
346. With the simultaneous cessation of irritation of the sympathetic and parasympathetic nerve fibers going to the heart, the effect of the sympathetic nerve lasts longer, because the activity of acetylcholinesterase is higher than the activity of monoamine oxidase (an enzyme that breaks down norepinephrine).
5) VVV
347. The tissues of internal organs are sensitive to mediators of postganglionic nerve fibers (norepinephrine, acetylcholine, histamine), because the membranes of tissue cells have adreno-, cholinergic-, histamine receptors.
5) VVV
348. Norepinephrine can cause both constriction and expansion of arterioles, because the effect of norepinephrine depends on the type of adrenoreceptors (alpha and beta) with which it interacts.
The phenomenon of the central braking was discovered by I. M. Sechenov in 1862. His main experience was as follows. An incision was made in the frog's brain at the level of the visual tubercles and removed large hemispheres. After that, the time of the withdrawal reflex of the hind legs was measured when they were immersed in a solution of sulfuric acid (Türk's method).
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This reflex is carried out by the spinal centers and its time is an indicator of the excitability of the centers. I. M. Sechenov discovered that if the cut of the visual tubercles ( rice. 177) to impose a crystal of table salt or apply a weak electrical stimulation to this area of the brain, then the time of the reflex is sharply lengthened. Based on this fact, I. M. Sechenov came to the conclusion that in the thalamic region of the frog's brain there are nerve centers that have inhibitory effects on spinal cord reflexes. IM Sechenov correctly assessed the importance of the phenomenon of central inhibition discovered by him and used it in his theoretical works to explain the physiological mechanisms of human behavior. Rice. 177. The brain of a frog and its cut line in the experiment of I. M. Sechenov. 1 - olfactory nerve; 2 - olfactory lobe; 3 - large hemispheres; 4 - visual tubercle; 5 - line of section of the brain; 6 - double colliculus; 7 - cerebellum; 8 - medulla oblongata and rhomboid fossa. |
Soon new facts were discovered, demonstrating the phenomena inhibition in the central nervous system. F. Goltz showed that in a frog the reflex of withdrawing the hind leg in response to its immersion in an acid solution can be inhibited by simultaneous strong mechanical stimulation of the second leg, for example, by squeezing it with tweezers. F. Goltz also established that the frog's croaking reflex, observed when pressing on the side walls of the body, is inhibited by irritation of the legs.
F. Goltz observed inhibition of spinal reflexes even after the removal of the thalamic region in frogs, and therefore he opposed the idea of the existence of special inhibitory centers in the brainstem. Goltz believed that inhibition can develop in any part of the neutral nervous system upon encountering two or more stimuli that evoke different reflexes.
Ch. Sherrington, N. E. Vvedensky, A. A. Ukhtomsky and many other researchers showed that braking plays an important role in the activity of all parts of the central nervous system.
Let us give some examples of intracentral inhibition from the works of Ch. Sherrington, who studied in detail the patterns of interaction between the processes of excitation and inhibition in the spinal cord of mammals.
In a cat with remote large hemispheres, the central cox n is irritated. popliteus, which causes a reflex contraction of the knee extensor muscle - m. vastus сrureus - opposite limb ( rice. 178). This reflex has a long aftereffect. If during it a second irritation is applied to the same n. popliteus, then there is inhibition of the previously evoked reflex and relaxation of the muscle.
Reflex contraction of the knee extensor muscle can be caused by irritation of the skin of the paw of the opposite side (extension cross reflex). The application of strong irritation to the skin of the paw of the same side is accompanied by a sharp reflex relaxation of this muscle due to the inhibition that has arisen in the centers of inhibition ( rice. 178). Similarly, the flexion reflex in a cat, caused by irritation of the nerve of the same side, is inhibited by irritation of the nerve or skin of the symmetrical side.
The intensity of reflex inhibition depends on the ratio of the strength of stimuli - the excitatory and inhibitory nerve center.
If the stimulus causing the reflex is strong and the inhibitory stimulus is weak, then the intensity of inhibition is low. With the opposite ratio of the strength of these irritations, the reflex will be completely inhibited.
If several weak inhibitory stimuli are applied to the nerve, then the inhibition is intensified, i.e., an increase in inhibitory influences is observed.
NE Vvedensky observed the phenomena of inhibition in the cerebral cortex. In his experiments, against the background of stimulation of a certain point in the motor zone of the cortex of one hemisphere (this caused bending of one of the paws on the opposite side of the body), a symmetrical point of the cortex of the other hemisphere was irritated. As a result, the effect of the first irritation was inhibited (the bent paw unbent).
IP Pavlov, who studied the inhibition of conditioned reflexes and showed that the phenomena of inhibition are important in all manifestations of the higher nervous activity and behavior of the organism, made a major contribution to the theory of central inhibition.
Various, outwardly contradictory views have been expressed on the question of the mechanism of central inhibition. Some researchers believed that in the central nervous system there are special structures specialized for the function of inhibition and that inhibition is, in its physicochemical nature, opposite to excitation. Others believed that inhibition in the central nervous system arises as a result of a conflict of several excitations or as a result of excessively strong or prolonged excitation ("overexcitation"), i.e., it develops according to the mechanism of Vvedesky's pessimum.
Modern electrophysiological studies by J. Eccles, D. Purpura, P. G. Kostyuk and others made it possible to establish that both investigators were right to a certain extent, since there are several types of inhibition in the central nervous system that have different nature and different localization.
- Pessimal inhibition in nerve centers. Inhibition of the activity of a nerve cell can be carried out without the participation of special inhibitory structures. In this case, inhibition develops in excitatory synapses as a result of a strong depolarization of the postsynaptic membrane under the influence of too frequent nerve impulses reaching it. The prototype of such inhibition is in the neuromuscular junction. Intermediate neurons of the spinal cord, neurons are especially prone to pessimal inhibition. reticular formation and some other cells in which the depolarization of the postsynaptic membrane during frequent rhythmic stimulation can be so intense and persistent that a state similar to cathodic development develops in the cell. .
- Inhibition followed by excitation. A special type of inhibition is inhibition that develops in a nerve cell after the cessation of its excitation. It occurs if, after the end of the excitation flash, a strong trace hyperpolarization of the membrane develops in the cell. The excitatory postsynaptic potential under these conditions is insufficient for the critical depolarization of the membrane, and propagating excitation does not occur.
Braking (physiology)
Braking- v physiology- active nervous process caused by excitement and manifested in the suppression or prevention of another wave of excitation. Provides (together with excitation) the normal activity of all organs and the body as a whole. It has a protective value (primarily for the nerve cells of the cerebral cortex), protecting nervous system from excitement.
I. P. Pavlov called irradiation braking by cerebral cortex head brain"the damned question of physiology."
Central braking
Central braking was discovered in 1862. I. M. Sechenov. In the course of the experiment, he removed the frog's brain at the level of the visual tubercles and determined the time of the flexion reflex. Then a crystal was placed on the visual tubercles salt as a result, an increase in the duration of the reflex time was observed. This observation allowed I. M. Sechenov to express his opinion about the phenomenon of inhibition in the central nervous system. This type of braking is called Sechenovskiy or central.
Ukhtomsky explained the results from a dominant position. In the visual tubercles - the dominant of excitation, which suppresses the action of the spinal cord.
Vvedensky explained the results in terms of negative induction. If excitation occurs in the central nervous system in a certain nerve center, then inhibition is induced around the focus of excitation. Modern explanation: when the visual tubercles are stimulated, the caudal section of the reticular formation is excited. These neurons excite the inhibitory cells of the spinal cord ( Renshaw cells), which inhibit the activity of alpha motor neurons in the spinal cord.
Primary braking
Primary inhibition occurs in special inhibitory cells adjacent to the inhibitory neuron. At the same time, inhibitory neurons secrete the corresponding neurotransmitters.
Types of primary braking
Reverse - the neuron affects the cell, which in response inhibits the same neuron.
Reciprocal - this is mutual inhibition, in which the excitation of one group of nerve cells ensures the inhibition of other cells through intercalary neuron.
Lateral - inhibitory cell inhibits nearby neurons. Similar phenomena develop between bipolar and ganglion cells retina, which creates conditions for a clearer vision of the subject.
Reverse facilitation - neutralization of neuron inhibition during inhibition of inhibitory cells by other inhibitory cells.
postsynaptic- the main type of primary inhibition, is caused by the excitation of Renshaw cells and intercalary neurons. With this type of inhibition, hyperpolarization of the postsynaptic membrane occurs, which causes inhibition. Examples of primary inhibition:
presynaptic- occurs in ordinary neurons, is associated with the process of excitation.
Secondary braking
Secondary inhibition occurs in the same neurons that generate excitation.
Types of secondary braking
Pessimal inhibition- this is a secondary inhibition that develops in excitatory synapses as a result of a strong depolarization of the postsynaptic membrane under the influence of multiple impulses.
Inhibition followed by excitation occurs in ordinary neurons and is also associated with the process of excitation. At the end of the act of excitation of a neuron, a strong trace hyperpolarization can develop in it. At the same time, the excitatory postsynaptic potential cannot bring the membrane depolarization to critical level of depolarization, voltage-gated sodium channels do not open and action potential does not occur.
Peripheral inhibition
Opened by the Weber brothers in 1845. An example is the inhibition of the activity of the heart (decrease heart rate) when irritated vagus nerve.
Conditional and unconditional inhibition
The terms "conditional" and "unconditional" inhibition were proposed by I. P. Pavlov.
Conditional inhibition
Conditioned, or internal, inhibition is a form of inhibition of a conditioned reflex that occurs when conditioned stimuli are not reinforced by unconditioned ones. Conditioned inhibition is an acquired property and is developed in the process of ontogeny. Conditioned inhibition is central inhibition and weakens with age.
Unconditional braking
Unconditional (external) inhibition - inhibition of a conditioned reflex that occurs under the influence of unconditioned reflexes (for example, orienting reflex). IP Pavlov attributed unconditioned inhibition to the innate properties of the nervous system, that is, unconditioned inhibition is a form of central inhibition.
Braking
The coordinating function of local neural networks, in addition to amplification, can also be expressed in the weakening of too intense activity of neurons due to their inhibition.
Fig. 8.1. Reciprocal (A), presynaptic (B) and reverse (C) inhibition in local neural circuits of the spinal cord
1 - motor neuron; 2 - inhibitory interneuron; 3 - afferent terminals.
Braking, as a special nervous process, is characterized by the lack of the ability to actively spread through the nerve cell and can be represented by two forms - primary and secondary inhibition.
Primary braking due to the presence of specific inhibitory structures and develops primarily without prior excitation. An example of primary inhibition is the so-called reciprocal inhibition of antagonist muscles found in the spinal reflex arcs. The essence of this phenomenon is that if the proprioreceptors of the flexor muscle are activated, then they simultaneously excite the motor neuron of this flexor muscle through the primary afferents and the inhibitory intercalary neuron through the collateral of the afferent fiber. Excitation of the interneuron leads to postsynaptic inhibition of the motor neuron of the antagonistic extensor muscle, on the body of which the axon of the inhibitory interneuron forms specialized inhibitory synapses. Reciprocal inhibition plays important role in automatic coordination of motor acts.
Another example of primary inhibition is open B. Renshaw return braking. It is carried out in a neural circuit, which consists of a motor neuron and an intercalary inhibitory neuron - Renshaw cells. Impulses from an excited motor neuron through the recurrent collaterals extending from its axon activate the Renshaw cell, which in turn causes inhibition of the discharges of this motor neuron. This inhibition is realized due to the function of inhibitory synapses that the Renshaw cell forms on the body of the motor neuron that activates it. Thus, a circuit with negative feedback is formed from two neurons, which makes it possible to stabilize the frequency of motor cell discharges and suppress excess impulses going to the muscles.
In some cases, Renshaw cells form inhibitory synapses not only on the motor neurons that activate them, but also on neighboring motor neurons with similar functions. The inhibition of surrounding cells carried out through this system is called lateral.
Inhibition according to the principle of negative feedback occurs not only at the output, but also at the input of the motor centers of the spinal cord. A phenomenon of this kind has been described in monosynaptic connections of afferent fibers with spinal motor neurons, the inhibition of which in this situation is not associated with changes in the postsynaptic membrane. The latter circumstance made it possible to define this form of inhibition as presynaptic. It is due to the presence of intercalary inhibitory neurons, to which collaterals of afferent fibers are suitable. In turn, intercalary neurons form axo-axonal synapses on afferent terminals that are presynaptic with respect to motor neurons. In the case of an excessive influx of sensory information from the periphery, inhibitory interneurons are activated, which, through axo-axonal synapses, cause depolarization of afferent terminals and, thus, reduce the amount of mediator released from them, and, consequently, the efficiency of synaptic transmission. An electrophysiological indicator of this process is a decrease in the amplitude of EPSPs recorded from the motor neuron. However, there are no signs of changes in ion permeability or generation of IPSP in motor neurons.
Question about mechanisms of presynaptic inhibition is quite complex. Apparently, the mediator in the inhibitory axo-axonal synapse is gamma-aminobutyric acid, which causes depolarization of afferent terminals by increasing the permeability of their membrane for C1- ions. Depolarization reduces the amplitude of action potentials in afferent fibers and thereby reduces the quantum release of the mediator in the synapse. Another possible cause of terminal depolarization may be an increase in the external concentration of K+ ions during prolonged activation of afferent inputs. It should be noted that the phenomenon of presynaptic inhibition was found not only in the spinal cord, but also in other parts of the CNS.
Investigating the coordinating role of inhibition in local neural circuits, one more form of inhibition should be mentioned - secondary inhibition, which arises without the participation of specialized inhibitory structures as a result of excessive activation of the excitatory inputs of the neuron. In the specialized literature, this form of inhibition is defined as braking of Vvedensky, who discovered it in 1886 in the study of the neuromuscular synapse.
Vvedensky inhibition plays a protective role and occurs with excessive activation of central neurons in polysynaptic reflex arcs. It is expressed in persistent depolarization of the cell membrane, which exceeds the critical level and causes inactivation of Na-channels responsible for the generation of action potentials. Thus, the processes of inhibition in local neural networks reduce excessive activity and are involved in maintaining optimal modes of impulse activity of nerve cells.
INHIBITION IN THE CNS. TYPES AND SIGNIFICANCE.
The manifestation and implementation of the reflex is possible only if the spread of excitation from one nerve center to another is limited. This is achieved by the interaction of excitation with another nervous process, which is opposite in effect to the process of inhibition.
Almost until the middle of the 19th century, physiologists studied and knew only one nervous process - excitation.
The phenomena of inhibition in the nerve centers, i.e. in the central nervous system were first discovered in 1862 by I.M. Sechenov ("Sechenov's inhibition"). This discovery played no less a role in physiology than the very formulation of the concept of a reflex, since inhibition is necessarily involved in all nervous acts without exception. And .M.Sechenov discovered the phenomenon of central inhibition during stimulation of the diencephalon of warm-blooded animals.In 1880, the German physiologist F.Goltz established the inhibition of spinal reflexes.N.E.Vvedensky, as a result of a series of experiments on parabiosis, revealed the intimate connection between the processes of excitation and inhibition and proved that nature these processes is one.
Braking - local nervous process leading to inhibition or prevention of excitation. Inhibition is an active nervous process, the result of which is the limitation or delay of excitation. One of the characteristic features of the inhibitory process is the lack of the ability to actively spread through the nervous structures.
Currently, two types of inhibition are distinguished in the central nervous system: central braking (primary), which is the result of excitation (activation) of special inhibitory neurons and secondary braking, which is carried out without the participation of special inhibitory structures in the very neurons in which excitation occurs.
Central braking ( primary) - a nervous process that occurs in the central nervous system and leads to the weakening or prevention of excitation. According to modern concepts, central inhibition is associated with the action of inhibitory neurons or synapses that produce inhibitory mediators (glycine, gamma-aminobutyric acid), which cause a special type of electrical changes on the postsynaptic membrane called inhibitory postsynaptic potentials (IPSP) or depolarization of the presynaptic nerve ending with which another nerve ending of the axon. Therefore, central (primary) postsynaptic inhibition and central (primary) presynaptic inhibition are distinguished.
Postsynaptic inhibition(Latin post behind, after something + Greek sinapsis contact, connection) - a nervous process due to the action on the postsynaptic membrane of specific inhibitory mediators (glycine, gamma-aminobutyric acid) secreted by specialized presynaptic nerve endings. The mediator secreted by them changes the properties of the postsynaptic membrane, which causes suppression of the cell's ability to generate excitation. In this case, a short-term increase in the permeability of the postsynaptic membrane to K+ or CI ions occurs, causing a decrease in its input electrical resistance and the generation of an inhibitory postsynaptic potential (IPSP). The occurrence of IPSP in response to afferent stimulation is necessarily associated with the inclusion of an additional link in the inhibitory process - an inhibitory interneuron, the axonal endings of which release an inhibitory neurotransmitter. The specificity of inhibitory postsynaptic effects was first studied in mammalian motor neurons (D. Eccles, 1951). Subsequently, primary IPSPs were recorded in interneurons of the spinal and medulla oblongata, in neurons of the reticular formation, cerebral cortex, cerebellum, and thalamic nuclei of warm-blooded animals.
It is known that when the center of the flexors of one of the limbs is excited, the center of its extensors is inhibited and vice versa. D. Eccles found out the mechanism of this phenomenon in the following experiment. He irritated the afferent nerve, causing excitation of the motor neuron that innervates the extensor muscle.
Nerve impulses, having reached the afferent neuron in the spinal ganglion, are sent along its axon in the spinal cord in two ways: to the motor neuron that innervates the extensor muscle, exciting it, and along the collaters to the intermediate inhibitory neuron, the axon of which contacts the motor neuron that innervates the flexor muscle, thus causing inhibition of the antagonistic muscle. This type of inhibition was found in intermediate neurons of all levels of the central nervous system during the interaction of antagonistic centers. He was named translational postsynaptic inhibition. This type of inhibition coordinates and distributes the processes of excitation and inhibition between the nerve centers.
Reverse (antidromic) postsynaptic inhibition(Greek antidromeo to run in the opposite direction) - the process of regulation by nerve cells of the intensity of the signals coming to them according to the principle of negative feedback. It lies in the fact that the collaterals of the axons of the nerve cell establish synaptic contacts with special intercalary neurons (Renshaw cells), whose role is to influence the neurons that converge on the cell that sends these axon collaterals (Fig. 87). According to this principle, inhibition of motor neurons.
The appearance of an impulse in a mammalian motor neuron not only activates muscle fibers, but also activates inhibitory Renshaw cells through axon collaterals. The latter establish synaptic connections with motor neurons. Therefore, an increase in motor neuron firing leads to greater activation of Renshaw cells, which causes increased inhibition of motor neurons and a decrease in the frequency of their firing. The term "antidromic" is used because the inhibitory effect is easily caused by antidromic impulses reflexively occurring in motor neurons.
The stronger the motor neuron is excited, the more strong impulses go to the skeletal muscles along its axon, the more intensely the Renshaw cell is excited, which suppresses the activity of the motor neuron. Therefore, there is a mechanism in the nervous system that protects neurons from excessive excitation. A characteristic feature of postsynaptic inhibition is that it is suppressed by strychnine and tetanus toxin (these pharmacological substances do not act on excitation processes).
As a result of the suppression of postsynaptic inhibition, the regulation of excitation in the central nervous system is disturbed, the excitation spills (“diffuses”) throughout the central nervous system, causing overexcitation of motor neurons and convulsive contractions of muscle groups (convulsions).
Reticular inhibition(lat. reticularis - mesh) - a nervous process that develops in spinal neurons under the influence of descending impulses from the reticular formation (giant reticular nucleus of the medulla oblongata). The effects created by reticular influences are functionally similar to the recurrent inhibition that develops on motor neurons. The influence of the reticular formation is caused by persistent IPSP, covering all motor neurons, regardless of their functional affiliation. In this case, as in the case of recurrent inhibition of motor neurons, their activity is limited. There is a certain interaction between such downward control from the reticular formation and the system of recurrent inhibition through Renshaw cells, and Renshaw cells are under constant inhibitory control from the two structures. The inhibitory influence from the reticular formation is an additional factor in the regulation of the level of motor neuron activity.
Primary inhibition can be caused by mechanisms of a different nature, not associated with changes in the properties of the postsynaptic membrane. Inhibition in this case occurs on the presynaptic membrane (synaptic and presynaptic inhibition).
synaptic inhibition(Greek sunapsis contact, connection) - a nervous process based on the interaction of a mediator secreted and secreted by presynaptic nerve endings with specific molecules of the postsynaptic membrane. The excitatory or inhibitory nature of the action of the mediator depends on the nature of the channels that open in the postsynaptic membrane. Direct proof of the presence of specific inhibitory synapses in the CNS was first obtained by D. Lloyd (1941).
Data regarding the electrophysiological manifestations of synaptic inhibition: the presence of synaptic delay, the absence electric field in the area of synaptic endings, they gave reason to consider it a consequence of the chemical action of a special inhibitory mediator secreted by synaptic endings. D. Lloyd showed that if the cell is in a state of depolarization, then the inhibitory mediator causes hyperpolarization, while against the background of hyperpolarization of the postsynaptic membrane, it causes its depolarization.
Presynaptic inhibition ( lat. prae - ahead of something + gr. sunapsis contact, connection) is a special case of synaptic inhibitory processes, manifested in the suppression of neuron activity as a result of a decrease in the effectiveness of excitatory synapses even at the presynaptic link by inhibiting the process of mediator release by excitatory nerve endings. In this case, the properties of the postsynaptic membrane do not undergo any changes. Presynaptic inhibition is carried out by means of special inhibitory interneurons. Its structural basis is axo-axonal synapses formed by axon terminals of inhibitory interneurons and axonal endings of excitatory neurons.
In this case, the axon ending of the inhibitory neuron is presympathetic with respect to the terminal of the excitatory neuron, which is postsynaptic with respect to the inhibitory ending and presynaptic with respect to the nerve cell activated by it. In the endings of the presynaptic inhibitory axon, a mediator is released, which causes depolarization of the excitatory endings by increasing the permeability of their membrane for CI. Depolarization causes a decrease in the amplitude of the action potential arriving at the excitatory ending of the axon. As a result, the mediator release process is inhibited by excitatory nerve endings and the amplitude of the excitatory postsynaptic potential decreases.
A characteristic feature of presynaptic depolarization is slow development and long duration (several hundred milliseconds), even after a single afferent impulse.
Presynaptic inhibition differs significantly from postsynaptic inhibition in pharmacological terms as well. Strychnine and tetanus toxin do not affect its course. However, narcotic substances (chloralose, nembutal) significantly enhance and lengthen presynaptic inhibition. This type of inhibition is found in various parts of the central nervous system. Most often it is detected in the structures of the brain stem and spinal cord. In the first studies of the mechanisms of presynaptic inhibition, it was believed that the inhibitory action is carried out at a point remote from the soma of the neuron, therefore it was called "remote" inhibition.
The functional significance of presynaptic inhibition, covering the presynaptic terminals through which afferent impulses arrive, is to limit the flow of afferent impulses to the nerve centers. Presynaptic inhibition primarily blocks weak asynchronous afferent signals and passes stronger ones, therefore, it serves as a mechanism for isolating, isolating more intense afferent impulses from the general flow. This is of great adaptive importance for the organism, since of all the afferent signals going to the nerve centers, the most important, the most necessary for a given specific time, stand out. Thanks to this, the nerve centers, the nervous system as a whole, are freed from the processing of less essential information.
Secondary braking- inhibition carried out by the same nervous structures in which excitation occurs. This nervous process is described in detail in the works of N.E. Vvedensky (1886, 1901).
reciprocal inhibition(lat. reciprocus - mutual) - a nervous process based on the fact that the same afferent pathways through which the excitation of one group of nerve cells is carried out provide inhibition of other groups of cells through the intercalary neurons. Reciprocal relations of excitation and inhibition in the central nervous system were discovered and demonstrated by N.E. Vvedensky: irritation of the skin on the hind leg in a frog causes its flexion and inhibition of flexion or extension on the opposite side. The interaction of excitation and inhibition is a common property of the entire nervous system and is found both in the brain and in the spinal cord. It has been experimentally proven that the normal performance of each natural motor act is based on the interaction of excitation and inhibition on the same CNS neurons.
General central braking - a nervous process that develops with any reflex activity and captures almost the entire central nervous system, including the centers of the brain. General central inhibition usually manifests itself before the occurrence of any motor reaction. It can manifest itself with such a small force of irritation at which there is no motor effect. This type of inhibition was first described by I.S. Beritov (1937). It provides a concentration of excitation of other reflex or behavioral acts that could arise under the influence of stimuli. An important role in the creation of general central inhibition belongs to the gelatinous substance of the spinal cord.
With electrical stimulation of the gelatinous substance in the spinal preparation of a cat, a general inhibition of reflex reactions caused by irritation of the sensory nerves occurs. General inhibition is an important factor in creating an integral behavioral activity of animals, as well as in ensuring selective excitation of certain working organs.
Parabiotic inhibition develops in pathological conditions, when the lability of the structures of the central nervous system decreases or there is a very massive simultaneous excitation of a large number of afferent pathways, as, for example, in traumatic shock.
Some researchers distinguish another type of inhibition - inhibition following excitation. It develops in neurons after the end of excitation as a result of a strong trace hyperpolarization of the membrane (postsynaptic).
Braking- an active process that occurs under the action of stimuli on the tissue, manifests itself in the suppression of another excitation, there is no functional administration of the tissue.
Inhibition can only develop in the form of a local response.
There are two braking type:
1) primary. For its occurrence, the presence of special inhibitory neurons is necessary. Inhibition occurs primarily without prior excitation under the influence of an inhibitory mediator. There are two types of primary inhibition:
presynaptic in the axo-axonal synapse;
postsynaptic at the axodendrial synapse.
2) secondary. It does not require special inhibitory structures, it arises as a result of a change in the functional activity of ordinary excitable structures, it is always associated with the process of excitation. Types of secondary braking:
beyond, arising from a large flow of information entering the cell. The flow of information lies outside the neuron's performance;
pessimal, arising at a high frequency of irritation; parabiotic, arising from strong and long-acting irritation;
inhibition following excitation, resulting from a decrease in the functional state of neurons after excitation;
braking by the principle of negative induction;
inhibition of conditioned reflexes.
The processes of excitation and inhibition are closely related, occur simultaneously and are different manifestations of a single process. The foci of excitation and inhibition are mobile, cover larger or smaller areas of neuronal populations, and may be more or less pronounced. Excitation will certainly be replaced by inhibition, and vice versa, i.e., there are inductive relations between inhibition and excitation.
Inhibition underlies the coordination of movements, protects the central neurons from overexcitation. Inhibition in the central nervous system can occur when nerve impulses of various strengths from several stimuli simultaneously enter the spinal cord. Stronger stimulation inhibits the reflexes that should have come in response to weaker ones.
In 1862, I. M. Sechenov discovered the phenomenon central braking. He proved in his experiment that irritation of the frog's optic tubercles with a sodium chloride crystal (the large hemispheres of the brain were removed) causes inhibition of spinal cord reflexes. After elimination of the stimulus, the reflex activity of the spinal cord was restored. The result of this experiment allowed I. M. Secheny to conclude that in the CNS, along with the process of excitation, a process of inhibition develops, which is capable of inhibiting the reflex acts of the body. N. E. Vvedensky suggested that the principle of negative induction underlies the phenomenon of inhibition: a more excitable section in the central nervous system inhibits the activity of less excitable sections.
Modern interpretation of the experience of I. M. Sechenov(I. M. Sechenov irritated the reticular formation of the brain stem): excitation of the reticular formation increases the activity of inhibitory neurons of the spinal cord - Renshaw cells, which leads to inhibition of α-motor neurons of the spinal cord and inhibits the reflex activity of the spinal cord.
inhibitory synapses formed by special inhibitory neurons (more precisely, their axons). The mediator can be glycine, GABA and a number of other substances. Usually, glycine is produced in synapses, with the help of which postsynaptic inhibition is carried out. When glycine as a mediator interacts with neuron glycine receptors, hyperpolarization of the neuron occurs ( TPSP) and, as a result, a decrease in the excitability of the neuron up to its complete refractoriness. As a result, excitatory influences provided through other axons become ineffective or ineffective. The neuron is switched off from work completely.
Inhibitory synapses open mainly chloride channels, which allows chloride ions to easily pass through the membrane. To understand how inhibitory synapses inhibit the postsynaptic neuron, we need to remember what we know about the Nernst potential for Cl- ions. We calculated that it is equal to approximately -70 mV. This potential is more negative than the resting membrane potential of the neuron, which is -65 mV. Therefore, the opening of chloride channels will facilitate the movement of negatively charged Cl- ions from the extracellular fluid inward. This shifts the membrane potential towards more negative values compared to rest, to about -70 mV.
The opening of potassium channels allows positively charged K+ ions to move outward, resulting in more negativity within the cell than at rest. Thus, both events (the entry of Cl- ions into the cell and the exit of K+ ions from it) increase the degree of intracellular negativity. This process is called hyperpolarization. An increase in the negativity of the membrane potential compared to its intracellular level at rest inhibits the neuron, therefore, the exit of negativity values beyond the initial resting membrane potential is called TPSP.
VNS provides extraorganic and intraorganic regulation of body functions and includes three components: 1) sympathetic; 2) parasympathetic; 3) metsympathetic.
The autonomic nervous system has a number of anatomical and physiological features that determine the mechanisms of its work.
Anatomical properties:
1. Three-component focal arrangement of nerve centers. The lowest level of the sympathetic section is represented by the lateral horns from the VII cervical to III-IV lumbar vertebrae, and the parasympathetic - by the sacral segments and the brain stem. The higher subcortical centers are located on the border of the nuclei of the hypothalamus (the sympathetic division is the posterior group, and the parasympathetic division is the anterior one). The cortical level lies in the region of the sixth-eighth Brodmann fields (motosensory zone), in which point localization of incoming nerve impulses is achieved. Due to the presence of such a structure of the autonomic nervous system, the work of internal organs does not reach the threshold of our consciousness.
2. The presence of autonomic ganglia. In the sympathetic department, they are located either on both sides along the spine, or are part of the plexus. Thus, the arch has a short preganglionic and a long postganglionic path. The neurons of the parasympathetic department are located near the working organ or in its wall, so the arc has a long preganglionic and short postganglionic path.
3. Effetor fibers belong to group B and C.
Physiological properties:
1. Features of the functioning of the autonomic ganglia. The presence of the phenomenon cartoons(simultaneous occurrence of two opposite processes - divergence and convergence). Divergence- the divergence of nerve impulses from the body of one neuron to several postganglionic fibers of another. Convergence- convergence on the body of each postganglionic neuron of impulses from several preganglionic ones. This ensures the reliability of the transmission of information from the central nervous system to the working body. An increase in the duration of the postsynaptic potential, the presence of trace hyperpolarization and synoptic delay contribute to the transmission of excitation at a speed of 1.5–3.0 m/s. However, the impulses are partially extinguished or completely blocked in the autonomic ganglia. Thus, they regulate the flow of information from the CNS. Due to this property, they are called nerve centers placed on the periphery, and the autonomic nervous system is called autonomous.
2. Features of nerve fibers. Preganglionic nerve fibers belong to group B and conduct excitation at a speed of 3-18 m/s, postganglionic nerve fibers belong to group C. They conduct excitation at a speed of 0.5–3.0 m/s. Since the efferent pathway of the sympathetic division is represented by preganglionic fibers, and the parasympathetic pathway is represented by postganglionic fibers, the speed of impulse transmission is higher in the parasympathetic nervous system.
Thus, the autonomic nervous system functions differently, its work depends on the characteristics of the ganglia and the structure of the fibers.
Sympathetic nervous system carries out innervation of all organs and tissues (stimulates work of the heart, increases the lumen of the respiratory tract, inhibits the secretory, motor and absorption activity of the gastrointestinal tract, etc.). It performs homeostatic and adaptive-trophic functions.
Her homeostatic role consists in maintaining the constancy of the internal environment of the body in an active state, i.e. the sympathetic nervous system is included in the work only when physical activity, emotional reactions, stress, pain effects, blood loss.
Adaptive-trophic function aimed at regulating the intensity of metabolic processes. This ensures the adaptation of the organism to the changing conditions of the environment of existence.
Thus, the sympathetic department begins to act in an active state and ensures the functioning of organs and tissues.
parasympathetic nervous system is a sympathetic antagonist and performs homeostatic and protective functions, regulates the emptying of hollow organs.
The homeostatic role is restorative and operates at rest. This manifests itself in the form of a decrease in the frequency and strength of heart contractions, stimulation of the activity of the gastrointestinal tract with a decrease in blood glucose levels, etc.
All protective reflexes rid the body of foreign particles. For example, coughing clears the throat, sneezing clears the nasal passages, vomiting causes food to be expelled, etc.
Emptying of hollow organs occurs with an increase in the tone of smooth muscles that make up the wall. This leads to the entry of nerve impulses into the central nervous system, where they are processed and sent along the effector path to the sphincters, causing them to relax.
Metsympathetic nervous system is a collection of microganglia located in the tissues of organs. They consist of three types of nerve cells - afferent, efferent and intercalary, therefore, they perform the following functions:
20. Functional features of the somatic and autonomic nervous system. Comparative characteristics of the sympathetic, parasympathetic and metasympathetic divisions of the autonomic nervous system.
The first and main difference between the ANS structure and the somatic structure is the location of the efferent (motor) neuron. In the SNS, the intercalary and motor neurons are located in the gray matter of the SC; in the ANS, the effector neuron is placed on the periphery, outside the SC, and lies in one of the ganglia - para-, prevertebral, or intraorgan. Moreover, in the metasympathetic part of the ANS, the entire reflex apparatus is completely located in the intramural ganglia and nerve plexuses of the internal organs.
The second difference concerns the exit of nerve fibers from the CNS. Somatic NIs leave the SC segmentally and cover with innervation at least three adjacent segments. The fibers of the ANS exit from three parts of the CNS (GM, thoracolumbar and sacral SM). They innervate all organs and tissues without exception. Most visceral systems have triple (sympathetic, para- and metasympathetic) innervation.
The third difference concerns the innervation of the somatic and ANS organs. Transection of the ventral roots of the SM in animals is accompanied by a complete regeneration of all somatic efferent fibers. It does not affect the arcs of the autonomic reflex due to the fact that its effector neuron is located in the para- or prevertebral ganglion. Under these conditions, the effector organ is controlled by the impulses of this neuron. It is this circumstance that emphasizes the relative autonomy of this section of the National Assembly.
The fourth difference relates to the properties of nerve fibers. In the ANS, they are mostly non-fleshy or thin fleshy, such as preganglionic fibers, the diameter of which does not exceed 5 microns. Such fibers belong to type B. Postganglionic fibers are even thinner, most of them are devoid of myelin sheath, they belong to type C. In contrast to them, somatic efferent fibers are thick, fleshy, their diameter is 12-14 microns. In addition, pre- and postganglionic fibers are characterized by low excitability. To evoke a response in them, a much greater force of irritation is needed than for motor somatic fibers. ANS fibers are characterized by a long refractory period and a large chronaxy. The speed of NI propagation along them is low and amounts to up to 18 m/s in preganglionic fibers, and up to 3 m/s in postganglionic fibers. The action potentials of the ANS fibers are characterized by a longer duration than in somatic efferents. Their occurrence in preganglionic fibers is accompanied by a prolonged trace positive potential, in postganglionic fibers - by a trace negative potential followed by prolonged trace hyperpolarization (300-400 ms).
provides intraorganic innervation;
are an intermediate link between the tissue and the extraorganic nervous system. Under the action of a weak stimulus, the metsympathetic department is activated, and everything is decided at the local level. When strong impulses are received, they are transmitted through the parasympathetic and sympathetic divisions to the central ganglia, where they are processed.
The metsympathetic nervous system regulates the work of smooth muscles that are part of most organs of the gastrointestinal tract, myocardium, secretory activity, local immunological reactions, etc.
The phenomenon of central inhibition was discovered by I.M. Sechenov in 1862. He discovered that if a crystal of sodium chloride is applied to the transverse section of the visual tubercles of a frog or a weak electric current is applied, then the time of the Türk reflex is sharply extended (the Türk reflex is bending the paw when it is immersed u into acid). Soon new facts were discovered demonstrating the phenomena of inhibition in the central nervous system. Goltz showed that the Turk reflex is inhibited when the other foot is squeezed with tweezers, Sherrington proved the presence of inhibition of the reflex contraction of the extensor during the flexion reflex. It was proved that in this case the intensity of reflex inhibition depends on the ratio of the strength of the excitatory and inhibitory stimuli.
In the central nervous system, there are several ways of inhibition, which have a different nature and different localization. but in principle based on one mechanism - an increase in the difference between the critical level of depolarization and the value of the membrane potential of neurons.
1. postsynaptic inhibition. inhibitory neurons . It has now been established that in the CNS, along with excitatory neurons, there are special inhibitory neurons. An example is the so-called. Renshaw cell in the spinal cord. Renshaw discovered that the axons of motor neurons, before exiting the spinal cord, give rise to one or more collaterals that terminate on special cells whose axons form inhibitory synapses on the motor neurons of this segment. Due to this, the excitation that occurs in the motor neuron propagates along the direct path to the periphery to the skeletal muscle, and activates the inhibitory cell along the collateral, which suppresses further excitation of the motor neuron. This is a mechanism that automatically protects nerve cells from excessive excitation. Inhibition, carried out with the participation of Renshaw cells, is called recurrent postsynaptic inhibition. The inhibitory mediator in Renshaw cells is glycine.
Nerve impulses arising from the excitation of inhibitory neurons do not differ from the action potentials of ordinary excitatory neurons. However, in the nerve endings of inhibitory neurons, under the influence of this impulse, a mediator is released that does not depolarize, but, on the contrary, hyperpolarizes the postsynaptic membrane. This hyperpolarization is recorded in the form of an inhibitory postsynaptic potential (IPSP) - an electropositive wave. IPSP weakens the excitatory potential and thus prevents the achievement of the critical level of membrane depolarization necessary for the occurrence of propagating excitation. Postsynaptic inhibition can be eliminated by strychnine, which blocks inhibitory synapses.
2.Posttetanic inhibition. A special type of inhibition is one that occurs if, after the end of excitation, a strong hyperpolarization of the membrane occurs in the cell. The excitatory postsynaptic potential under these conditions is insufficient for the critical depolarization of the membrane and the generation of propagating excitation. The reason for this inhibition is that trace potentials are capable of summation, and after a series of frequent pulses, a summation of a positive trace potential occurs.
3.Pessimal inhibition. Inhibition of the activity of a nerve cell can be carried out without the participation of special inhibitory structures. In this case, it occurs in excitatory synapses as a result of a strong depolarization of the postsynaptic membrane under the influence of too frequent impulses (as a pessimum in a neuromuscular preparation). Interneurons of the spinal cord, neurons of the reticular formation, are particularly prone to pessimal inhibition. With persistent depolarization, a state similar to Verigo's cathodic depression sets in.
4.presynaptic inhibition. It was discovered relatively recently in the CNS, therefore, it has been studied less. Presynaptic inhibition is localized in the presynaptic terminals in front of the synaptic plaque. The axon endings of other nerve cells are located on the presynaptic terminals, forming axo-axonal synapses here. Their mediators depolarize the membrane of the terminals and bring them into a state similar to Verigo's cathodic depression. This causes a partial or complete blockade of the conduction of excitatory impulses along the nerve fibers going to the nerve endings. Presynaptic inhibition is usually prolonged.
