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General Neurophysiology

General Neurophysiology. Axonal transport Degeneration and regeneration in the nervous system Transduction of signals at the cellular level Reflex arch Central pattern generator. Axonal transport. (axoplasmatic transport) Anterograde

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General Neurophysiology

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  1. General Neurophysiology Axonal transport Degeneration and regeneration in the nervous system Transduction of signals at the cellular level Reflex arch Central pattern generator

  2. Axonal transport (axoplasmatic transport) Anterograde Proteosynthesis in the cell body only (ER, Golgi apparatus) Retrograde Moving the chemical signals from periphery

  3. Anterogradeaxonal transportfast (100 - 400 mm/day)MAP kinesin/mikrotubulesmoves neurotransmittersin vesicles and mitochondriaslow (0,5 – 10 mm/day)unknown mechanism structural components (cytoskeleton - aktin, myosin, tubulin), metabolic componentsRetrograde axonal transportfast (50 - 250 mm/day) MAP dynein/ mikrotubulesold mitochondria, vesicles (pinocytosis, receptor-mediated endocytosis in axon terminals, transport of e.g. growths factors),

  4. Axonal transport in the pathogenesis of diseases Rabies virus Replicates in muscle cell Axon terminal (endocytosis) Retrograde transport to the cell body Neurons produce copies of the virus CNS – behavioral changes Neurons innervating the salivary glands (anterograde transport) Tetanus toxin (produced by Clostridium tetani) Toxin is transported retrogradely in nerve cells Tetanus toxin is released from the nerve cell body Taken up by the terminals of neighboring neurons

  5. Axonal transport as a research tool Tracer studies Anterogradeaxonal transport Radioactively labeled amino acids (incorporated into proteins, transported in an anterograde direction, detectedby autoradiography) Injection into a group of neuronal cell bodies can identify axonal distribution Retrograde axonal transport Horseradish peroxidase is injected into regions containing axon terminals. Is taken up and transported retrogradely to the cell body. After histology preparationcan be visualized. Injection to axon terminalscan identify cell body

  6. Degeneration and regeneration in the nervous system • Neurons do not proliferate • Exceptions • - olfactory epithelium • - dentatum gyrus (stem cells) • - olfactory bulb • Generaly • Lost neurons are not replaced (proliferation of glia, astrocytic scar)

  7. Myelin sheath of axons in PNS(a membranous wrapping around the axon)

  8. Myelin sheath of axons in PNS(a basal lamina) Basal lamina

  9. Myelin sheath formation in CNS

  10. Injury of the axon in PNS • Compression, crushing, cutting – degeneration of the distal axon - but the cell body remains intact (Wallerian degeneration, axon is removedby macrophages) • Schwann cells remainand their basal lamina (band of Büngner) • Proximal axon sprouts (axonal sprouting) • Prognosis quo ad functionem • Compression, crushing –goodSchwann cells remain in their original orientation, axons can find their original targets • Cutting – worse, regeneration is less likely to occure

  11. Injury of the axon in PNS • Amputation of the limb • Proximal stumpfail to enter the Schwann cell tube, instead ending blindly in connective tissue • Blind ends rolle themselves into a ball and form aneuroma – phantom pain

  12. Injury of the axon in CNS • Oligodendrocytes do not create a basal lamina and a band of Büngner • Regeneration to a functional state is impossible Trauma of the CNS • proliferation and hypertrophy of astrocytes, astrocytic scar

  13. Transduction of signals at the cellular level • Axonal part –action potential, spreading without decrement, all-or-nothing law • Somatodendritic part – passive conduction of the signal, with decrement

  14. Axon – the signal is carried without decrement

  15. Dendrite and cell body – signal is propagated with decrement

  16. Signal propagation from dendrite to initial segment

  17. Origin of the APelectrical stimulusneurotransmitter on synapses

  18. Axonal part of the neuronAP – voltage-gated Ca2+ channels –neurotransmitter release Arrival of an AP in the terminal opens voltage-gated Ca2+ channels, causing Ca2+ influx, which in turn triggers transmitter release.

  19. Somatodendritic part of neuron Receptors on the postsynaptic membrane • Excitatory receptors open Na+, Ca2+channelsmembrane depolarization • Inhibitoryreceptors open K+, Cl-channels membrane hyperpolarization • EPSP – excitatory postsynaptic potential • IPSP – inhibitory postsynaptic potential

  20. Excitatory and inhibitory postsynaptic potential

  21. Interaction of synapses

  22. Summation of signals spatial and temporal

  23. Transduction of signals at the cellular level EPSP IPSP Initial segment AP Ca2+ influx Neurotransmitter Neurotransmitter releasing

  24. EPSP IPSP Neuronal activity in transmission of signals Discharge configurationsof various cells

  25. 1.AP, activation of the voltage-dependent Na+ channels (soma, area of the initial segment) 2. ADP, after-depolarization, acctivation of a high threshold Ca2+ channels, localized in the dendrites 3.AHP, after-hyperpolarization, Ca2+ sensitive K+ channels 4.Rebound depolarization, low threshold Ca2+ channels, de-inactivated during the AHP, activated when the depolarization decreases (probably localized at the level of the soma Influence of one cell on the signal transmission Threshold RMP

  26. Reflex arch Knee-jerk reflex

  27. Research on reflexes Ivan Petrovich Pavlov Russia nobelist 1904 Sir Charles Scott Sherrington Great Britain nobelist 1932

  28. Behavior as a chain of reflexes? LOCUST Two pairs of wings Each pair beat in synchrony but the rear wings lead the front wings in the beat cycle by about 10% Proper delay between contractions of the front and rear wing muscles

  29. Donald Wilson’s Experiment in 1961

  30. To confirm the hypothesis Identify the reflexes that are responsible for the flight pattern Deafferentaion = the elimination of sensory input into the CNS Remove sense organs at the bases of the wings Cut of the wings Removed other parts of locust s body that contained sense organs Unexpected result Motor signals to the flight muscles still came at the proper time to keep the wings beat correctly synchronized

  31. Extreme experiment Reduced the animal to a head and the floor of the thorax and the thoracic nerve cord Elecrodes on the stumps of the nerves that had innervated the removed flight muscles Motor pattern recorded in the absence of any movement of part of animal – fictive pattern Locust flight systém did not require sensory feedback to provide timing cues for rhythm generation Network of neurons Oscillator, pacemaker, central pattern generator

  32. Central pattern generator Model of the CPG for control of muscles during swimming in lamprey

  33. Central pattern generators A network of neurons capable of producing a properly timed pattern of motor impulses in the absence of any sensory feedback. Swimming Wing beating Walking Gallop, trot Licking Scratching Breathing

  34. Summary

  35. Axonal transport (axoplasmatic transport) Anterograde Proteosynthesis in the cell body only (ER, Golgi apparatus) Retrograde Moving the chemical signals from periphery

  36. Degeneration and regeneration in the nervous system • Damaged (differenciated) neurons are not replaced Trauma of the CNS – glial scarf • Axons in CNS • Axons in PNS

  37. Transduction of signals at the cellular level EPSP IPSP Initial segment AP Ca2+ influx Neurotransmitter Neurotransmitter releasing

  38. Central pattern generators Pacemakers Reflex arch

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