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Physiology of the Neuromuscular Junction

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A brief overview of the physiology of the neuromuscular junction.It includes a video towards the end sourced from the internet with the copyright watermarks intact.

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Physiology of the Neuromuscular Junction

  1. 1. Physiology of The Neuromuscular Junction Presented by: Dr. Ashwin Haridas
  2. 2. Neuromuscular Junction (NMJ) Junction between a motor neuron and its muscle fibre A synapse Motor end plate
  3. 3. The Motor Unit  Each motor neuron from the ventral horn runs uninterrupted up to the muscle  Splits into a functional group called the motor unit  Single neuron supplying a group of muscle fibres  Contract and relax as a unit
  4. 4. Anatomy The NMJ
  5. 5. Anatomy  Branching nerve terminals invaginate into the surface of the muscle fibre but lie outside the sarcolemma  Hence the synaptic cleft  Usually around 20-30 nm  ACh receptors on the post junctional membrane
  6. 6. Acetylcholine receptors  Nicotinic  Cation channels  Junctional or mature  Extra junctional or immature or fetal  Usually after muscle fibre injury  Within 18 hours  Altered response to NMJ blocking drugs  Sodium & Calcium moves in  Potassium moves out
  7. 7. The Immature Receptor  Increased sensitivity to depolarizing agents  Decreased sensitivity to non-depolarizing agents  Stays open for a longer time  Hence increased efflux of intracellular potassium  Altogether can cause lethal hyperkalemia
  8. 8. ACh (Synthesis, storage, release)  Synthesized in the Presynaptic terminal from substrate Choline and Acetyl CoA. CAT CHOLINE + ACETYL CoA ACETYL CHOLINE COMT 50% Carrier Facilitated Transport Release CHOLINE + ACETYL CoA ACETYL CHOLINE Synaptic Cleft
  9. 9.  Different subsets of ACh vesicles  Immediately releasable stores, VP2:  Responsible for the maintainence of transmitter release under conditions of low nerve activity  1% of vesicles  The reserve pool, VP1:  Released in response to nerve impulses  80% of vesicles  The stationary store: The remainder of the vesicles.
  10. 10. Acetylcholine  One vesicle contains approx. 12,000 molecules of ACh  Loaded by active transport- Mg2+ dependent H+ ATPase  A single vesicle equals a quantum ACh.
  11. 11. Nerve impulse reaches the terminal Calcium channels open up Ca2+ moves into the terminal Stimulates exocytosis of ACh vesicles at the active site
  12. 12. Replenishing the vesicles  Discharged vesicles are rapidly replaced from reserve stores  Reserve vesicles anchored to cytoskeletal actin by syanpsins  Ca2+ entry during initial discharge process also binds to calmodulin  Stimulates protein kinase-2 which phosphorylates synapsins  Reserve vesicles are thus freed
  13. 13.  Docking of the vesicle and subsequent discharge of acetylcholine by exocytosis, involves several other proteins.  Membrane protein called SNAREs (Soluble N-ethylmatrimide sensitive attachment proteins) are involved in fusion, docking, and release of acetylcholine at the active zone.  SNARE includes – synaptic vesicle protein synaptobrevin, synataxin and SNAP-25.
  14. 14.  The released acetylcholine diffuses to the muscle type nicotinic acetylcholine receptors which are concentrated at the tops of junctional folds of membrane of the motor end plate.  Binding of acetylcholine to these receptors increases Na and K conductance of membrane and resultant influx of Na produces a depolarising potential, end plate potential.  The current created by the local potential depolarise the adjacent muscle membrane to firing level.
  15. 15. ACh binds to nicotinic receptors Increases Na+ and K+ conductance Depolarising end plate potential is produced Depolarises the adjacent sarcolemma to firing level
  16. 16.  Acetylcholine is then removed by acetylcholinesterase from synaptic cleft, which is present in high concentration at NMJ.  Action potential generated on either side of end plate and are conducted away from end plate in both directions along muscle fiber.  The muscle action potential in turn initiates muscle contraction
  17. 17. The Sodium Channel  Cylindrical  Its two ends act as gates  Both should be open to allow passage of ions  Voltage dependent gate is closed in resting state and opens only on application of a depolarizing voltage, remains open as long as the voltage persists
  18. 18.  The time dependent gate is normally open at rest closing a few milliseconds after the voltage gate opens and remains closed as long as the voltage gate is open  It reopens after the voltage gate closes.  The channel is patent, allowing sodium ions only when the gates are open.
  19. 19. Na channel states • Resting state: Voltage gate closed Time gate open Channel closed • Depolarization: Voltage gate open Time gate open Channel open • Within a few milliseconds: Voltage gate open Time gate closed Channel closed • End of depolarization: Voltage gate closed Time gate open Channel closed
  20. 20. The Role of Calcium  The concentration of calcium and the length of time during which it flows into the nerve ending, determines the number of quanta released.  Calcium current is normally stopped by the out flow of potassium.  Calcium channels are specialized proteins, which are opened by voltage change accompanying action potentials
  21. 21.  Part of calcium is captured by proteins in the endoplasmic reticulum & is sequestrated.  Remaining part is removed out of the nerve by the Na/Ca antiport system  The sodium is eventually removed from the cell by ATPase
  22. 22. Acetylcholinesterase  This protein enzyme is secreted from the muscle, but remain attached to it by thin stalks of collagen, attached to the basement membrane.  Acetylcholine molecules that don’t interact with receptors are released from the binding site & are destroyed almost immediately by acetylcholinesterase, in <1 ms, after its release into the junctional cleft.
  23. 23. Extra ocular muscles  Tonic muscles  Multiple neuronal endings on a single muscle fibre  Contains immature receptors also  Reaction to depolarizing relaxant  Normal muscle – brief contraction followed by paralysis  Instead there is a long lasting contracture response  Pulls the eye against the orbit  Raises the IOP
  24. 24. Contractile apparatus  Thick and thin filaments  Actin  Myosin  Troponin  Tropomyosin  Calcium  The sarcomere
  25. 25. References  Miller’s Anesthesia, 7th edition  Clinical Anesthesiology by Morgan, Mikhail and Murray, 4th edition  Ganong’s Review of Medical Physiology, 23rd edition  Guyton and Hall: Textbook of Medical Physiology, 12th edition
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A brief overview of the physiology of the neuromuscular junction.It includes a video towards the end sourced from the internet with the copyright watermarks intact.

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