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Updated: Nov 3 2021

Action Potential Conduction

Images action potential.jpg potential propagation.jpg
  • Snapshot
    • A 36-year-old male presents with ascending muscle weakness. The patient is generally healthy, with no pertinent past medical history. He states he recently recovered from diarrhea that has lasted over a week. Neurological examination is notable for weakness in the lower extremities and an abscence of patellar reflexes. (Botulinum toxin)
  • Introduction
    • Action Potential Overview
      • initiation
        • neuronal membrane potential becomes more positive → opening of voltage gated Na+ channels
          • positive feedback loop
          • threshold is reached → action potential generated
      • propagation
        • action potential generated at one portion of neuron → excitation of adjacent neuronal membrane
          • signal thus propagates down the axon via opening of voltage gated Na+ channels
      • neuromuscular junction
        • when the propagated action potential reaches the presynaptic neuron, it becomes depolarized
          • this opens voltage gated Ca2+ channels
            • allows release of acetylcholine (ACh) from stored vesicles in the presynaptic neuron
        • released ACh act on nicotinic receptors (a ligand-gated ion channel) on the motor end plate
          • motor end plate depolarizes, and propagates the action potential down the muscle fiber, ultimately leading to muscle contraction
  • Action Potential Initiation
    • Initiation
      • initial depolarization → opening of voltage gated Na+ channels
        • increased Na+ inflow → opening of more voltage gated Na+ channels (positive feedback loop)
          • threshold is eventually met → action potential generation
        • clinical correlate
          • tetrodotoxin (pufferfish consumption) binds fast voltage-gated Na+ channels in nerve tissue, which does not allow for depolarization or action potential formation
            • can result in nausea, weakness, dizziness or can be fatal
            • treatment is supportive
  • Action Potential Propagation
    • Propagation
      • depolarized region of the neuronal membrane → excitation of adjacent neuronal membrane
      • myelinated neurons
        • Schwann cells myelinates axons of the peripheral nervous system (PNS)
          • myelinates only 1 axon
          • increases conduction velocity
          • non-myelinated areas are called Nodes of Ranvier
            • contains a high concentration of Na+ channels
              • allows "jumping" of action potential from one Node of Ranvier to the next
                • this is saltatory conduction
          • clinical correlate
            • Guillain-Barre syndrome
              • autoimmune destruction of peripheral myelinated neurons
                • classically associated with previous Campylobacter jejuni infection
        • myelinated neuron examples
          • sensory
            • Pacinian corpuscles transmit vibrational sense and pressure via large, myelinated fibers
      • non-myelinated neurons
        • transmit potentials via Na+ channels that exist along the entire length of the axon (no Nodes of Ranvier)
          • have same refractory period of Na+ channels as myelinated axons do but at a slower velocity of conduction due to lack of insulation (myelin)
  • Neuromuscular Junction
    • Neuromuscular junction
      • propagated action potential reaches presynaptic neuron → opens voltage gated Ca2+ channels
        • clinical correlate
          • Lambert-Eaton syndrome
            • autoantibodies against the presynaptic calcium channels → reduced ACh release → weakness
            • associated with small cell carcinoma of the lung
      • Ca2+ influx → ACh release with the help of SNARE proteins
        • clinical correlate
          • botulinum toxin
            • cleaves SNARE proteins → decreased ACh release → flaccid paralysis
          • tetanus toxin
            • cleaves SNARE proteins → decrease release of inhibitory neurotransmitters (GABA and glycine) in the spinal cord → spasticity and overactivity
      • released ACh act on nicotinic receptors (ligand gated ion channels) of the motor end plate
        • clinical correlate
          • myasthenia gravis
            • autoantibodies bind the post-synaptic ACh receptor → weakness
      • depolarization travels along the muscle cell via T-tubules, which are invaginations that allow for the skeletal muscle to be depolarized
      • dihydropyridine receptors are then depolarized
        • mechanically coupled to ryanodine receptors (Ca2+ release channels) on the sarcoplasmic reticulum
          • increases intracellular Ca2+ concentration → binds to troponin C → cross bridge cycle
            • See Skeletal and Cardiac Muscle Contractions topic
          • clinical correlate
            • malignant hyperthermia
              • ryanodine or dihydropyridine receptor mutation → unregulated Ca2+ release into the muscle cytoplasm → sustained muscle contraction → increased aerobic metabolism → depletion of O2, ATP, and increased CO2 production and acidosis
              • treatment: dantrolene
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