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      Functional Nicotinic Acetylcholine Receptors That Mediate Ganglionic Transmission in Cardiac Parasympathetic Neurons

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          Abstract

          Nicotinic acetylcholine receptors (nAChRs) mediate ganglionic transmission in the peripheral autonomic nervous system in mammals. Functional neuronal nAChRs have been shown to assemble from a combination of α and β subunits, including α3, α5, α7, β2, and β4 in RNA-injected oocytes, but the subunit composition of functional neuronal nAChRs in vivo in mammals remains unknown. We examined the subunit composition of functional nAChRs in the intracardiac parasympathetic ganglion in a physiologically intact system in vivo. We report here that localized perfusion of the canine intracardiac ganglion in situ with an antagonist specific for nAChRs containing an α3/β2 subunit interface (α-conotoxin MII 100–200 n m) resulted in reversible attenuation of the sinus cycle length (SCL) response by ∼70% to electrical stimulation of the preganglionic vagus nerve. Perfusion with antagonist specific for receptors containing an α3/β4 subunit interface (α-conotoxin AuIB 1 μ m) resulted in attenuation in SCL responses (∼20%) compared with baseline when applied by itself, but not in animals pretreated with α-conotoxin MII. Perfusion of the ganglion with α-bungarotoxin (1 μ m, which blocks α7 receptors) caused a reduction in SCL response by ∼30% compared with baseline when perfused on its own and when added after blockade with MII and AuIB. Perfusion with hexamethonium bromide resulted in complete blockade of ganglionic transmission, confirming total perfusion of the ganglion and the nicotinic nature of ganglionic transmission at this synapse. Immunohistochemistry using monoclonal antibodies against specific nicotinic subunits confirmed the presence of α3, α7, β2, and β4 subunits. We conclude that functional ganglionic transmission in the canine intracardiac ganglion is mediated primarily by receptors containing an α3/β2 subunit interface, with a smaller contribution by receptors containing α7 nAChRs. Despite the presence of β4 subunits in functional channels, a contribution of a distinct α3/β4 receptor population that does not include an α3/β2 subunit interface was less clear.

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          Author and article information

          Journal
          J Neurosci
          J. Neurosci
          jneuro
          jneurosci
          J. Neurosci
          The Journal of Neuroscience
          Society for Neuroscience
          0270-6474
          1529-2401
          1 July 2000
          : 20
          : 13
          : 5076-5082
          Affiliations
          [ 1 ]Departments of Physiology and Biophysics and
          [ 2 ]Neurosciences, Case Western Reserve University, Cleveland, Ohio 44106,
          [ 3 ]Departments of Biology and Psychiatry, University of Utah, Salt Lake City, Utah 84112, and
          [ 4 ]Department of Medicine–Cardiology, Veterans Affairs Medical Center, Cleveland, Ohio 44106
          Article
          PMC6772271 PMC6772271 6772271 4272
          10.1523/JNEUROSCI.20-13-05076.2000
          6772271
          10864965
          e81d72af-f663-4926-8aa7-cd67f63f099a
          Copyright © 2000 Society for Neuroscience
          History
          : 13 January 2000
          : 5 April 2000
          : 11 April 2000
          Categories
          ARTICLE
          Behavioral/Systems
          Custom metadata
          5.00

          acetylcholine,ganglion,cardiac,parasympathetic,neuronal,α-conotoxin,nicotinic receptor

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