Inhibition in cns 1


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Inhibition in cns 1

  1. 1. Volgograd State Medical Univercity Normal physiology Depertment Inhibition in the Central nervous system Rodion A. Kudrin
  2. 2. Plan <ul><li>Definition of inhibition </li></ul><ul><li>Classifications of inhibition. </li></ul><ul><li>Central (Sechenov's) inhibition. </li></ul><ul><li>Direct (postsynaptic) inhibition. </li></ul><ul><li>Reciprocal inhibition. </li></ul><ul><li>Renshaw inhibition. </li></ul><ul><li>Indirect (presynaptic) inhibition. </li></ul><ul><li>Pessimal inhibition. </li></ul><ul><li>Inhibition following excitation. </li></ul><ul><li>Lateral inhibition. </li></ul>
  3. 3. 1. Definition of I nhibition <ul><li>1. Inhibition means to slow down the excitation effect of the CNS. </li></ul><ul><li>2. Inhibition is the process whereby nerves can retard or prevent the functioning of an organ or part; &quot;the inhibition of the heart by the vagus nerve&quot;. </li></ul><ul><li>3. Inhibition is the reduction of a reflex or other activity as the result of an antagonistic stimulation. </li></ul><ul><li>4. Inhibition is a state created at synapses making them less excitable by other sources of stimulation. </li></ul>
  4. 4. 2. Classifications of inhibition <ul><li>Direct (postsynaptic) </li></ul><ul><li>Indirect (presynaptic) </li></ul><ul><li>1. Lateral </li></ul><ul><li>2. Reciprocal </li></ul><ul><li>3. Renshaw </li></ul><ul><li>4. Inhibition following excitation </li></ul><ul><li>5. Pessimal </li></ul><ul><li>1. Unconditioned </li></ul><ul><li>2. Conditioned </li></ul>
  5. 5. 3. Central inhibition (Sechenov's inhibition) <ul><li>The phenomenon of central inhibition was discovered by Sechenov in 1862 . </li></ul>Ivan M. Sechenov
  6. 6. 3. Central inhibition (Sechenov's inhibition) <ul><li>Sechenov's fundamental experiment was as follows: </li></ul><ul><li>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 . </li></ul>
  7. 7. 3. Central inhibition (Sechenov's inhibition) <ul><li>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. </li></ul><ul><li>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. </li></ul>
  8. 8. 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
  9. 9. 4. Postsynapti c inhibition <ul><li>It has now been established that there are so-called neurones both in the spinal cord and in different parts of the brain, in addition to excitatory neurones. The axons of these neurones form nerve endings in the bodies and dendrites of the excitatory cells, secreting a special inhibitory mediator (in the opinion of some researchers, it is gamma-aminobutyric acid and glycine ). </li></ul>
  10. 10. 4. Postsynapti c inhibition
  11. 11. 4. Postsynapti c inhibition
  12. 12. 4. Postsynapti c inhibition <ul><li>The nerve impulses generated by stimulation of inhibitory neurones do not differ from the action potentials of ordinary neurones, but an impulse arriving at the nerve endings of the former along the axon causes the secretion of a mediator which does not depolarize the postsynaptic membrane, but, on the contrary, hyperpolarizes it. The hyperpolarization is registered in the form of an electrically positive wave described as the postsynaptic potential. </li></ul>
  13. 13. 4. Postsynapti c inhibition
  14. 14. 4. Postsynapti c inhibition <ul><li>Like excitatory potentials, the inhibitory potentials arising in individual synapses may be summated spatially or in time, so that an increase in the strength of the stimuli inhibiting nerve centres leads to a rise in the inhibitory potential. </li></ul><ul><li>In each nerve cell there are numerous excitatory and inhibitory synapses in close proximity to one another, which provides favourable conditions for their interaction. </li></ul>
  15. 15. 4. Postsynapti c inhibition
  16. 16. 4. Postsynapti c inhibition
  17. 17. 4. Postsynapti c inhibition <ul><li>The inhibitory postsynaptic potential weakens the excitatory potential, thereby preventing attainment of the critical level of depolarization required to trigger spreading excitation. When, therefore, stimulation of an afferent nerve producing inhibition is a little ahead of the exciting stimulus in time, an action potential will not arise in the nerve cell, but if the inhibitory stimulus is applied after excitation has already begun, i. e. in the presence of rhythmic discharges of impulses, then the impulses will come less frequently, or will be terminated completely. </li></ul>
  18. 18. 4. Postsynapti c inhibition
  19. 19. 4. Postsynapti c inhibition <ul><li>The degree of inhibition of a cell depends on the ratio of the magnitudes of the excitatory and inhibitory potentials, and on the number of synapses of both types involved in the reaction. </li></ul><ul><li>If the exciting potential is of suprathreshold value, while the inhibitory potential is low, then, despite its weakening, the former may still prove sufficient for a critical depolarization of the neurone membrane and the appearance of spreading excitation. With an increased inhibitory potential critical depolarization under the influence of an excitatory stimulus becomes impossible. </li></ul>
  20. 20. 4. Postsynapti c inhibition <ul><li>The magnitude of the inhibitory postsynaptic potential is quickly reduced in time (with a single stimulation it does not last longer than ten milliseconds), so that, with an increase in the interval between the two types of stimulus, the inhibitory effect is weakened. </li></ul>
  21. 21. 4. Postsynapti c inhibition <ul><li>The stronger a reflex, i. e. the larger number of nerve cells taking part in its initiation, the greater strength of inhibitory stimulus requires to suppress it. </li></ul><ul><li>The type of inhibition described here is called , because it is due to hyperpolarization of the postsynaptic membrane. A distinctive feature is that it can be removed by strychnine, which blocks the inhibitory synapses. </li></ul>
  22. 22. 5. R eciprocal inhibition <ul><li>Consider, the basic stretch reflex. When the muscle concerned, (Mp – muscle protagonist) is stretched, the afferent nerve fiber, AF – afferent fiber is stimulated and AF makes direct synapse with the efferent nerve cell soma, Sp. Now the efferent nerve fiber is stimulated and the muscle Mp contracts. </li></ul>
  23. 23. 5. R eciprocal inhibition
  24. 24. 5. R eciprocal inhibition <ul><li>AF also gives collateral ac, which synapses with a different nerve cell soma. The axon of this soma is the motor neuron to the antagonist muscle Ma. When the AF is stimulated, the collateral is also stimulated but the result of the collateral stimulation is development of IPSP at the termination of the collateral, (due to liberation of proper chemical transmitter at this synapse) so that the nerve fiber supplying the antagonistic muscle is inhibited (so that the antagonist muscle Ma is relaxed). The phenomenon is also called, ' reciprocal inhibition ' (of Sherrington). </li></ul>
  25. 25. 5. R eciprocal inhibition <ul><li>The teleologic 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. </li></ul>
  26. 26. 6. Renshaw inhibition <ul><li>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. </li></ul>
  27. 27. 6. Renshaw cell inhibition <ul><li>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. </li></ul>
  28. 28. 6. Renshaw cell inhibition
  29. 29. 6. Renshaw cell inhibition <ul><li>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. </li></ul>
  30. 30. 7. Presynapti c inhibition <ul><li>As its name implies, this type of inhibition is localized in the presynaptic elements, namely, the finest arborizations of the axons before they enter the nerve ending. These arborizations, or terminals, incorporate the endings of other nerve cells, forming specific synapses. The mediators (GABA) secreted in these inhibitory synapses depolarize the membrane of the terminals and bring them in a state similar to Werigo's cathodal depression which results in a partial or complete block of conduction of impulses to the nerve endings. </li></ul>
  31. 31. 7. Presynapti c inhibition
  32. 32. 7. Presynapti c inhibition <ul><li>Axon 'e' of a neuron, which is excitatory is impinging on the soma, V of a second neuron. Thus, there is a synapse, shown by a red circle, between e and s. When e is excited s is also excited. </li></ul><ul><li>Another axon, i, is impinging on e and thus there is another synapse, shown by a red circle between the termination of e and i. Mark, this synapse is axoaxionic (= between two axons). The presynaptic membrane i has inhibitory effect on the e. </li></ul>
  33. 33. 7. Presynapti c inhibition <ul><li>When i is silent, stimulation of e causes excitation of s. But where i is stimulated, i releases GABA, which causes hyperpolarization of e and as a result the synaptic transmission from e to s is stopped. Instead of severe hyperpolarization, there may be milder degrees of hyperpolarization (of e), so that, when both i and e are stimulated, only weak EPSPs are generated in the s and no AP develops (in the s). </li></ul>
  34. 34. 7. Presynapti c inhibition
  35. 35. 8. Pessimal inhibition in the nerve centres <ul><li>The activity of a nerve cell can be inhibited without the participation of special inhibitory structures. In that case, inhibition develops in the excitatory synapses as a result of strong depolarization of the postsynaptic membrane under the influence of nerve impulses arriving too frequently. </li></ul>
  36. 36. 8. Pessimal inhibition in the nerve centres <ul><li>The prototype of this inhibition is Vvedensky's pessimum in the myoneural junction. The internuncial neurones of the spinal cord are particularly liable to Vvedensky's inhibition and so are the neurones of the reticular formation and certain other cells in which depolarization of the postsynaptic membrane during a frequent rhythmic stimulation may be so intensive and persistent as to develop a state similar to Werigo's cathodal depression in the cell. </li></ul>
  37. 37. 9. Inhibition following excitation <ul><li>A discrete type of inhibition is that developing in a nerve cell after termination of excitation and which appears when excitation is followed by strong after-hyperpolarization of the cell membrane. The excitatory postsynaptic potential arising under these conditions proves insufficient to depolarize the membrane, so that a spreading of excitation does not occur. </li></ul>
  38. 38. 10. Lateral inhibition <ul><li>A simple form of information processing. The classic example is found in the eye, whereby ganglion cells are stimulated if photoreceptors in a well defined field are illuminated, but their response is inhibited if neighbouring photoreceptors are excited (an on field/off surround cell) or vice versa an off field/on surround cell. The effect of lateral inhibition is to produce edge or boundary sensitive cells and to reduce the amount of information that is sent to higher centres, a form of peripheral processing. </li></ul>
  39. 39. 6. Lateral inhibition
  40. 40. <ul><li>Thank you for your attention! </li></ul>