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Electrophysiological and Pharmacological Characterization of the NANC Nerve Mediated Inhibition of the Circular Muscle Layer of the Opossum Esophagus

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Abstract

Field stimulation of strips from the circular muscle of the esophagus of the North American opossum induced a transient nerve mediated hyperpolarization of the smooth muscle cell membrane (IJP), followed by an “off” depolarization, usually accompanied by spike activity and muscle contraction. Optimum stimulus parameters were 0.1 to 0.2 ms pulse duration and 20 pps for 0.3 s. Tetrodotoxin and scorpion venom abolished responses at these parameters.

These responses were unaffected by atropine, guanethidine or indomethacin in effective doses. ATP, ADP, AMP and adenosine had no consistent effects on membrane potential or on the IJP in concentrations up to 10−4 M. VIP from 10−8 M upward caused enhanced “off” depolarization and initiated spontaneous activity.

Manipulation of external potassium ion concentration and of membrane potential effected the IJP amplitude consistent with its origin from increased conductance towards potassium ions. Double sucrose gap studies showed that during the IJP the membrane resistance decreased. A conditioning hyperpolarization of more than about 40 mV reversed the IJP. This reversal potential of the IJP was dependent on the potassium concentation of the super fusion medium. Thus the IJP seems to be due to a selective increase in the permeability of the smooth muscle cell membrane towards potassium ions.

Apamine up to 10−5M did not affect the membrane potential or the IJP. Tetraethylammonium (TEA) 1 — 3 x 10−2M induced a depolarization of muscle cell membrane and increased the membrane resistance and increased the IJP. These results suggest that the potassium channels of the smooth muscle cell membrane in this preparation are apamine-insensitive and probably voltage-regulated.

However, the potassium channels opened by the inhibitory neurotransmitter are qualitatively different from those functioning at rest. Like TEA, quinine (10−3M) induced a depolarization at rest, but unlike TEA it did block the IJP. This effect may be due to an interference of quinine with the conductance change underlying the IJP or with the impulse propagation by the intramural nerves.

The pharmacological properties of the potassium channels in the opossum esophagus employed by the inhibitory transmitter are unlike those of other smooth muscle preparations of the gastrointestinal tract.

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Jager, L.P., Jury, J., Daniel, E.E. (1984). Electrophysiological and Pharmacological Characterization of the NANC Nerve Mediated Inhibition of the Circular Muscle Layer of the Opossum Esophagus. In: Roman, C. (eds) Gastrointestinal Motility. Springer, Dordrecht. https://doi.org/10.1007/978-94-010-9352-1_2

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  • DOI: https://doi.org/10.1007/978-94-010-9352-1_2

  • Publisher Name: Springer, Dordrecht

  • Print ISBN: 978-94-010-9354-5

  • Online ISBN: 978-94-010-9352-1

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