Kursk State Medical UnivercityNormal physiology Depertment

Inhibition in theCentral nervous system

Gustavo Duarte V.Zotova Oksana M.Group: 17

Plan

Definition of Inhibition Roles of Inhibition Explain what is the EPSP and IPSP Inhibitory transmitters Mechanism of Gaba Classifications of inhibition according the localization Mechanism and Properties of the inhibitory postsynaptic

potential Mechanism of presynaptic inhibition Classification of Inhibition

1. Lateral

2. Reciprocal

3. Renshaw

4. Inhibition following excitation

5. Pessimal

Classification of Inhibition by nature Classification by mechanism Coordination Principal of coordination Convergence of signal Divergence of signal Successive and simultaneous induction Reciprocity Occlusion Facilitation Principal of final common pathway Principal of feedback The principle of dominant Central Inhibition of CNS (Sechenov’s experiment) References

1. Definition of Inhibition

1. Inhibition in a general definition is a Indendent nerve process which is caused by exitation & manifested by the suppression of another exitation.

2. Inhibition means to slow down the excitation effect of the CNS.

3. Inhibition is the process whereby nerves can retard or prevent the functioning of an organ or part; "the inhibition of the heart by the vagus nerve".

4. Inhibition is the reduction of a reflex or other activity as the result of an antagonistic stimulation.

5. Inhibition is a state created at synapses making them less excitable by other sources of stimulation.

Roles of inhibition

Protection (E.g. as antaganism protection)

Coordination ( Inhibition of nervous process in the CNS that ensures tha harmonious activity)

Explain what is EPSP and IPSP

EPSP: Excitatory post synaptic membrane, this moves the cell toward the threshold level by allowing positive ions to enter in the cell as result of opening the ligand ions channels. The larger the EPSP the more like the action potention is to fire.

IPSP: Inhibitory post synaptic membrane. It moves the cell away from the threshold level due to the movement of negative ions into the cell or positive ions out of the cell.

Inhibitory transmitters

Gaba: is used at the great majority of fast inhibitory synapses in virtually every part of the brain. Many sedative/tranquilizing drugs act by enhancing the effects of GABA.

Glycine is Correspondingly as GABA, but is the inhibitory transmitter in the spinal cord

Dopamine: has a number of important functions in the brain. It plays a critical role in the reward system, but dysfunction of the dopamine system is also implicated in Parkinson's disease and schizophrenia.

Mechanism of GABA

GABA is the major inhibitory neurotransmitter in the CNS. GABA is present stored in vesicles. Given a certain stimulus, GABA is released into the synaptic cleft to act on their specific receptors in the postsynaptic neuron, and after it activity is reuptake. the action of GABA on its receptors results in membrane hyperpolarization.

GABA and its receptors are widely distributed in mammalian CNS.

The completion of the actions of GABA at the synaptic cleft (reuptake) is performed through specific transporters located in the membrane of presynaptic terminals and glial cells, and their catabolism is performed by the enzyme GABA-transaminase (GABA-T). the action of GABA-T, converts-ketoglutarate to L-glu by transamination,and then the L-glu is converted to glutamine by the action of glutamine synthetase, to be transported from glial cell to the presynaptic neuron. In the presynaptic neuron, the glutaminase converts glutamine to L-glu, and it undergoes the action of glutamate decarboxylase to produce and stock GABA in vesicles.

2. Classifications of inhibition according the localization• Direct (postsynaptic)• Indirect (presynaptic)

Mechanism and Properties of the inhibitory postsynaptic potential

Increase in negativity beyond normal resting potential level.

The inhibitory mainly open to Cl ions -70 mvolt . more –ve than -65 mvolt that present inside resting neuronal membrane.

Opening Cl channel allow negatively charge Cl ion to move from extracellular fluid --> interior --> will make interior membrane potential more negative than normal.

Opening of K channel allow positively charge K ion to move from interior --> extracellular --> also will make interior membrane potential more negative. 

Both Cl influx and K influx increase the degree of intracellular negativity – hyperpolarization.

It inhibit neuron because : membrane potential father away from -45 mv threshold for excitation.

IPSP --> - 5 mv.

4. Postsynaptic inhibition

Postsynaptic inhibition

Mechanism of presynaptic inhibition

Occur at presynaptic terminal before the signal ever reach the synapse.

inhibition in presynaptic cause : i. Discharge of inhibitory synapse that lie on the outside of the

presynaptic terminal nerve fibrils before their ending terminate on postsynaptic neuron.

ii. The inhibitory transmitter released is GABA (gamma-amino butyric acid )

--> Specific effect of opening anion channel . allowing large no. Cl ion to

diffuse into terminal fibril. - the negative charge of these ion cancel excitatory effect of

positive charge Na ion that enter terminal fibril when AP arrival. --> the positively increase in postsynaptic is reduce thus reducing excitation of synapse.

- it occur in many sensory pathway in nervous system. - terminal nerve fiber inhibit one another , minimize the

sideway spread of signal in sensory tract.

Classification of Inhibition

1. Lateral2. Reciprocal3. Renshaw4. Inhibition following excitation5. Pessimal

Lateral Inhibition

Is a mechanism that is used through the nervous system to sharpen signal transmission.

This process uses inhibition of the input from the peripheral of the receptive field to better define the boundaries of the exited zone.

Motor system & Sensory system use this mechanism to focus and sharpen its signals. E.G.: Eyes

Picture showing the lateral inhibition

Reciprocal Inhibition

When the central nervous system sends a message to the agonist (muscle causing movement) to contract, the tension in the antagonist (muscle opposing movement) is inhibited by impulses from motor neurons, and thus must simultaneously relax. This neural phenomenon is called reciprocal inhibition.

The teleological principle is obvious. When a group of muscles, say, the flexors of the elbow contract the opposing (antagonist) muscles, (extensors of the elbow in this example), must relax to ensure flexion.

Renshaw inhibition

From the big sized anterior horn cells of the spinal cord, emerge Aα motoneurons which end in the skeletal muscles. Now, upper motor neuron or cortico spinal (pyramidal) tract fibers impinge on these Aα motoneurons. Therefore, when the corticospinal tract fires, Aα motoneurons are stimulated.

Renshaw cell inhibition

Collaterals from the Aα motoneurons emerge and impinge upon cells, called Renshaw cells. When the Aα fibers are stimulated, the Renshaw cells, therefore, are also stimulated. The axon of the Renshaw cell now inhibit the nerve cell soma of the Aα neurons.

Renshaw cell inhibition

This phenomenon is called Renshaw cell inhibition (after Renshaw, who discovered it in 1946). The teleology of this phenomenon appears to be to produce a condition so that even if the corticospinal tract fires repetitively, the frequency of the muscle contraction remains less (Renshaw cell inhibition lasts for quite a few milli seconds), and thus the muscle is protected against too high frequency stimuli.

Pessimal inhibition

inhibition developes in the excitatory synapses as a result of strong depolarization of the Post-synaptic membrane under the influence of nerve impulses arriving too frequently.

The intermediate neuron of Spinal Cord neurons of the reticular formation are particularly liable to pessimal inhibition.

Classification of Inhibition by nature

Prymary inhibition “In time” E.G renshaw cells

Protection in case o f Hyperpolarization coordination

Secondary inhibition ” after excitation”

Classification by mechanism Hyperpolarization Depolarization: Prolonged

depolarization produce pessimum inhibition in nerve center

= Reticular formation of the brain stem

= Interneurons of spinal cord

Coordination

The principle of coordinationCoordination – harmonization of the activity

of nervous centers

CoordinationCoordination

ConvergenceConvergence DivergenceDivergence ReverberatioReverberationn

summationAlleviationOcclusionCommonterminalway

IrradiationGeneralizationInductionReciprocalinteraction

Aftereffect

Convergence of signal

from different source from same source  impulses reaching the CNS, along

different afferent fibers that may convert upon the same intermediate or effectors neuron

Eg. Auditory, skin, muscle

Divergence of signal

neuron cell establish numerous synaptic contracts w diff. nerve cells. this phenomena known as divergence

spread of excitation through the CNS is known irradiation

Coordination principle

Sucessive and simultaneous induction

Negative successive induction + → -Positive successive induction -→ +Negative simultaneous == + --Positive simultaneous ++=++

* the phenomena were attributed to stimulation of the nerve centers of flexor muscular channel of 1 leg inhibition of the center of extensor muscular channel of the same leg & excitation of the center of the extensors key in the other legexcitation of the center of 1 group of muscles in accompany w a reciprocal inhibition of the centers of antagonist group of muscles

Reciprocity

the phenomena were attributed to stimulation of the nerve centers of flexor muscular channel of 1 leg inhibition of the center of extensor muscular channel of the same leg & excitation of the center of the extensors key in the other leg

excitation of the center of 1 group of muscles in accompany w a reciprocal inhibition of the centers of antagonist group of muscles

Occlusion

consist simultaneously stimulation of 2 groups of afferent fibers, discharge zone, producing an effect whose magnitude is less than arimethical sum of reflexes taken separately

Facilitation

consist in simultaneous stimulation of 2 groups of afferent fibers at facilitated zone, producing an effect whose magnitude is bigger than the arthmyatical sum of those reflexes taken separately

Principal of final common path way

One and the same motor neuron involve in many reflex arch

Effector neuron form a final common pathways for reflexes of different origin & can be linked w any of the organism receptor

The principle of feedback Afferent impulsation generated

within the org. by the activity of its organ & tissues can be called secondary in contrast to these first elicited & reflex reaction

Secondary affrentation send impulsations in the CNS about state of motor apparatus about state of excitatory gland.?feedback afferentation

The principle of dominantDominant – is the dominant center of excitation

in CNS, modifying and subordinates a work of other centers, it is the basic working principal of nervous system

Meaning of dominant:Meaning of dominant:1.1. Ensure the formation of behavioral reactionsEnsure the formation of behavioral reactions

2.2. Ensure the formation of emotionsEnsure the formation of emotions

3.3. Participation in the pathogenesis Participation in the pathogenesis of diseasesof diseases

Properties of dominant:Properties of dominant:1.1. Increased excitabilityIncreased excitability

2.2. Persistence of excitationPersistence of excitation

3.3. Ability to summationAbility to summation

4.4. Ability to brakeAbility to brake

5.5. InertiaInertia

Conditions of formation of dominant: Influence of environmental stimuli Influence of stimuli of the internal environment

(level of nutrients, hormones)

Conditions of disappearance of Conditions of disappearance of dominant:dominant:

Meeting the needs for which formed Meeting the needs for which formed dominantdominant

The emergence of a stronger dominantThe emergence of a stronger dominant Secondary braking in dominantSecondary braking in dominant

3. Central inhibition (Sechenov's inhibition)

The phenomenon of central inhibition was discovered by Sechenov in 1862.

Ivan M. Sechenov

Central inhibition (Sechenov's inhibition)

Sechenov's fundamental experiment was as follows:

a frog brain as incised at the level of the thalamus, and the cerebral hemispheres removed. Then the reflex time for withdrawing the hind legs from a solution of sulphuric acid was measured (Turck's method). The reflex was performed by the spinal centers and its time indicated their excitability.

3. Central inhibition (Sechenov's inhibition)

Sechenov found that application of a crystal of common salt or a weak electrical stimulus to the section of the thalamus markedly prolonged the reflex time. From this experiment he concluded that there were nerve centers in the thalamic region of the frog brain producing an inhibitory influence on spinal reflexes.

Sechenov correctly evaluated the great importance of the phenomenon of central inhibition he had discovered, and used it in his theoretical work to explain the physiological mechanisms of man's behaviour.

3. Central inhibition (Sechenov's inhibition)A frog brain showing the line of section in Sechenov's expiriment1 - olfactory nerve;

2 – olfactory lobe;

3 – cerebral hemispheres;

4 – thalamus;

5 – line of brain section;

6 – corpora bigemina;

7 – cerebellum;

8 – medulla oblongata and fossa rhomboidea

Central inhibition by ICentral inhibition by I..MM.. Sechenov Sechenov

References

▶ Lecture of Prof. Avdeev Elena V.▶ Arthur C. Guyton, M.D. Physiology,

Eleventh Edition

Thank you for attention…