Acetylcholine-activated ionic currents in isolated paratracheal ganglion cells of the rat.
The electrophysiological property of acetylcholine (ACh)-induced current (IACh) was studied in paratracheal ganglion cells freshly isolated from rat trachea under whole-cell voltage-clamp condition. IACh consisted of an initial transient peak component and a successive steady-state plateau one. The peak component increased in a sigmoidal fashion with increasing ACh concentration. The IACh was mimicked by nicotine. The current-voltage relationship for the IACh showed inward rectification at the positive membrane potentials beyond the reversal potential (EACh). In a K(+)-free solution, the EACh was close to the Na+ equilibrium potential. The IACh was blocked by either D-tubocurarine or atropine. The ion selectivity of ACh-activated channels to various monovalent cations was weak, and similar to those of other preparations. It was concluded that the IACh in rat paratracheal ganglion cells was mediated by nicotinic receptor activation.
Aibara
K
K
Department of Neurophysiology, Tohoku University School of Medicine, Sendai, Japan.
Akaike
N
N
D000109:Acetylcholine / Q000494:pharmacology*; D000818:Animals; D001285:Atropine / Q000494:pharmacology; D002469:Cell Separation; D004594:Electrophysiology; D005110:Extracellular Space / Q000378:metabolism; D005724:Ganglia / Q000166:cytology / Q000378:metabolism / Q000502:physiology*; D007473:Ion Channels / Q000378:metabolism; D010277:Parasympathomimetics / Q000494:pharmacology; D051381:Rats; D012964:Sodium / Q000378:metabolism; D014132:Trachea / Q000294:innervation*; D014403:Tubocurarine / Q000494:pharmacology
D007473:Ion Channels; D010277:Parasympathomimetics; D001285:Atropine; D012964:Sodium; D000109:Acetylcholine; D014403:Tubocurarine