Inhibition of the central nervous system


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Inhibition of the central nervous system.

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  • 19/10/09 23:11
  • 19/10/09 23:11
  • 19/10/09 23:11
  • 19/10/09 23:11
  • 19/10/09 23:11
  • 19/10/09 23:11
  • 19/10/09 23:11
  • 19/10/09 23:11
  • 19/10/09 23:11
  • 19/10/09 23:11
  • 19/10/09 23:11
  • 19/10/09 23:11
  • Inhibition of the central nervous system

    1. 1. Kursk State Medical Univercity Normal physiology Depertment Inhibition in theCentral nervous system Gustavo Duarte V. Zotova Oksana M. Group: 17
    2. 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. 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. 4. 1. Definition of Inhibition1. 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. 5. Roles of inhibition Protection (E.g. as antaganism protection) Coordination ( Inhibition of nervous process in the CNS that ensures tha harmonious activity)
    6. 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. 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 Parkinsons disease and schizophrenia.
    8. 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.
    9. 9. 2. Classifications of inhibition according the• localization Direct (postsynaptic)• Indirect (presynaptic)
    10. 10. Mechanism and Properties of theinhibitory 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.
    11. 11. 4. Postsynaptic inhibition
    12. 12. Postsynaptic inhibition
    13. 13. 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.
    14. 14. Classification of Inhibition1. Lateral2. Reciprocal3. Renshaw4. Inhibition following excitation5. Pessimal
    15. 15. 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
    16. 16. Picture showing the lateralinhibition
    17. 17. 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.
    18. 18. Renshaw inhibitionFrom 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.
    19. 19. Renshaw cell inhibitionCollaterals 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.
    20. 20. Renshaw cell inhibitionThis 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.
    21. 21. 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.
    22. 22. Classification of Inhibition by naturePrymary inhibition “In time” E.G renshaw cells Protection in case o f Hyperpolarization coordinationSecondary inhibition ” after excitation”
    23. 23. Classification by mechanism Hyperpolarization Depolarization: Prolonged depolarization produce pessimum inhibition in nerve center= Reticular formation of the brain stem= Interneurons of spinal cord
    24. 24. Coordination
    25. 25. The principle of coordinationCoordination – harmonization of the activity of nervous centers CoordinationConvergence Divergence Reverberationsummation Irradiation AftereffectAlleviation GeneralizationOcclusion InductionCommon Reciprocalterminal interactionway
    26. 26. 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
    27. 27. 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
    28. 28. Coordination principle
    29. 29. flexor muscular channel of 1 leg inhibition of the center of extensor muscular channel of the samcal inhibition of the centers of antagonist group of muscles Sucessive and simultaneous induction Negative successive induction + → - Positive successive induction -→ + Negative simultaneous == + -- Positive simultaneous ++=++
    30. 30. 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
    31. 31. 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
    32. 32. 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
    33. 33. 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
    34. 34. 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
    35. 35. 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 systemMeaning of dominant:1. Ensure the formation of behavioral reactions2. Ensure the formation of emotions3. Participation in the pathogenesis of diseasesProperties of dominant:1. Increased excitability2. Persistence of excitation3. Ability to summation4. Ability to brake5. Inertia
    36. 36. Conditions of formation ofdominant:  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
    37. 37. 3. Central inhibition(Sechenovs inhibition)The phenomenon of central inhibition was discovered by Sechenov in 1862. Ivan M. Sechenov
    38. 38. Central inhibition (Sechenovsinhibition)Sechenovs 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 (Turcks method). The reflex was performed by the spinal centers and its time indicated their excitability.
    39. 39. 3. Central inhibition(Sechenovs 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 mans behaviour.
    40. 40. 3. Central inhibition(Sechenovsinhibition)A frog brain showing the lineof section in Sechenovsexpiriment1 - olfactory nerve;2 – olfactory lobe;3 – cerebral hemispheres;4 – thalamus;5 – line of brain section;6 – corpora bigemina;7 – cerebellum;8 – medulla oblongata and fossarhomboidea
    41. 41. Central inhibition by I.M. Sechenov
    42. 42. References▶ Lecture of Prof. Avdeev Elena V.▶ Arthur C. Guyton, M.D. Physiology, Eleventh Edition
    43. 43. Thank you for attention…