An acetylcholine-induced potassium current in tail sensory neurons in the pleural ganglion of Aplysia.
Acetylcholine (ACh) induces a hyperpolarization during current clamp and an outward current during voltage clamp in tail sensory neurons of Aplysia kurodai. This response was proved to be produced by a specific increase in membrane permeability toward potassium ions, the cholinergic antagonists, d-tubocurarine chloride (d-TC), and atropine mildly reduced the ACh response, while tetraethylammonium (TEA) most effectively blocked this response. These findings provide evidence that tail sensory neurons have the inhibitory ACh receptor in addition to the known receptors for serotonin (5-HT), small cardioactive peptide B (SCPB), and neuropeptide Phe-Met-Arg-Phe-NH2 (FMRFamide).
Ichinose
M
M
Department of Physiology, Shimane Medical University, Japan.
Sawada
M
M
Maeno
T
T
D000109:Acetylcholine / Q000494:pharmacology*; D000818:Animals; D001048:Aplysia; D001285:Atropine / Q000494:pharmacology; D002478:Cells, Cultured; D005724:Ganglia / Q000502:physiology; D008564:Membrane Potentials / Q000187:drug effects; D009475:Neurons, Afferent / Q000187:drug effects / Q000502:physiology*; D015221:Potassium Channels / Q000187:drug effects / Q000502:physiology*; D019789:Tetraethylammonium; D013757:Tetraethylammonium Compounds / Q000494:pharmacology; D014403:Tubocurarine / Q000494:pharmacology
D015221:Potassium Channels; D013757:Tetraethylammonium Compounds; D019789:Tetraethylammonium; D001285:Atropine; D000109:Acetylcholine; D014403:Tubocurarine