This document outlines a plan for a presentation on inhibition in the central nervous system. It will define inhibition, describe the roles of inhibition in protection and coordination. It will explain excitatory and inhibitory postsynaptic potentials and the major inhibitory neurotransmitters like GABA. It will classify inhibition by location, mechanism, and nature. It will cover topics like lateral, reciprocal, and Renshaw inhibition. It will also discuss Sechenov's pioneering experiment demonstrating central inhibition in the brain. References will be included.

1. Kursk State Medical Univercity
Normal physiology Depertment
Inhibition in the
Central nervous system
Gustavo Duarte V.
Zotova Oksana M.
Group: 17

2. 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

3.  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

4. 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.

5. Roles of inhibition
 Protection (E.g. as antaganism protection)
 Coordination ( Inhibition of nervous process
in the CNS that ensures tha harmonious
activity)

6. 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.

7. 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.

8. 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.

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

11. 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.

12. 4. Postsynaptic inhibition

13. Postsynaptic inhibition

14. 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.

16. Classification of
Inhibition
1. Lateral
2. Reciprocal
3. Renshaw
4. Inhibition following excitation
5. Pessimal

17. 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

18. Picture showing the lateral
inhibition

19. 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.

21. 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.

22. 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.

23. 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.

24. 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.

25. Classification of Inhibition by
nature
Prymary inhibition “In time” E.G renshaw cells
Protection in case o f Hyperpolarization
coordination
Secondary inhibition ” after excitation”

26. Classification by mechanism
 Hyperpolarization
 Depolarization: Prolonged depolarization
produce pessimum inhibition in nerve center
= Reticular formation of the brain stem
= Interneurons of spinal cord

27. Coordination

28. The principle of coordination
Coordination – harmonization of the activity of
nervous centers
Coordination
Convergence Divergence Reverberation
summation
Irradiation Aftereffect
Alleviation
Generalization
Occlusion
Induction
Common
Reciprocal
terminal
interaction
way

29. 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

30. 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

31. Coordination principle

32. flexor muscular channel of 1 leg inhibition of the center of extensor muscular channel of the sam
cal inhibition of the centers of antagonist group of muscles
Sucessive and simultaneous induction
Negative successive induction + → -
Positive successive induction -→ +
Negative simultaneous == + --
Positive simultaneous ++=++

33. 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

34. 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

35. 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

36. 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

37. 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

38. The principle of dominant
Dominant – 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:
1. Ensure the formation of behavioral reactions
2. Ensure the formation of emotions
3. Participation in the pathogenesis of diseases
Properties of dominant:
1. Increased excitability
2. Persistence of excitation
3. Ability to summation
4. Ability to brake
5. Inertia

39. Conditions of formation of
dominant:
 Influence of environmental stimuli
 Influence of stimuli of the internal environment
(level of nutrients, hormones)
Conditions of disappearance of dominant:
 Meeting the needs for which formed dominant
 The emergence of a stronger dominant
 Secondary braking in dominant

40. 3. Central inhibition
(Sechenov's inhibition)
The phenomenon of
central inhibition was
discovered by
Sechenov in 1862.
Ivan M. Sechenov

41. 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.

42. 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.

43. 3. Central inhibition
(Sechenov's
inhibition)
A frog brain showing the line
of section in Sechenov's
expiriment
1 - 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

44. Central inhibition by I.M. Sechenov

45. References
▶ Lecture of Prof. Avdeev Elena V.
▶ Arthur C. Guyton, M.D. Physiology, Eleventh
Edition

46. Thank you for attention…