Presynaptic M2 muscarinic receptors are involved in controlling the kinetics of ACh release at the frog neuromuscular junction

Authors

  • I. Slutsky,

    1. The Otto Loewi Minerva Center for Cellular and Molecular Neurobiology, Department of Neurobiology, The Hebrew University, Jerusalem
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  • I. Silman,

    1. Department of Neurobiology, The Weizmann Institute, Rehovot, Israel
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  • I. Parnas,

    1. The Otto Loewi Minerva Center for Cellular and Molecular Neurobiology, Department of Neurobiology, The Hebrew University, Jerusalem
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  • H. Parnas

    Corresponding author
    1. The Otto Loewi Minerva Center for Cellular and Molecular Neurobiology, Department of Neurobiology, The Hebrew University, Jerusalem
    • Corresponding author
      I. Parnas: The Otto Loewi Minerva Center for Cellular and Molecular Neurobiology, Department of Neurobiology, The Hebrew University, Jerusalem, Israel. Email: ruthy@vms.huji.ac.il

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Abstract

  • 1Macropatch recording was used to study release of acetylcholine in the frog neuromuscular junction evoked by either direct local depolarization or by an action potential.
  • 2The quantal content was established by directly counting the released quanta. The time course of release was obtained by constructing synaptic delay histograms.
  • 3Perfusion of the neuromuscular junction with methoctramine, a selective M2/M4 muscarinic antagonist, increased the quantal content and slowed the exponential decay of the synaptic delay histograms. Addition of the agonist muscarine reversed these effects.
  • 4Addition of acetylcholinesterase prolonged the decay of the delay histogram, and muscarine reversed this effect.
  • 5Methoctramine slowed the rise time of the postsynaptic current produced by axon stimulation without affecting either the excitatory nerve terminal current or the presynaptic Ca2+ current.
  • 6These results show that presynaptic M2 muscarinic receptors are involved in the process which terminates evoked ACh release.

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