Calcium-dependent slow outward current in visceral primary afferent neurones of the rabbit.
Slow outward currents were recorded from voltage-clamped neurones in nodose ganglia excised from rabbits. In the majority of Type C neurones, a short depolarizing command pulse evoked a slow outward tail current (ISAH) with a decay time constant ranging from 0.5 to 2 s. The ISAH was due to an increase in membrane conductance to K+ because its reversal potential was approximately equal to the Nernst potential for K+. The ISAH was reversibly blocked by removal of external Ca2+ or by Ca2+ antagonists. A Ca2+ ionophore, A23187, produced an outward current which was similar to the ISAH. The ISAH was resistant to tetraethylammonium and depressed by Ba2+, whereas it was not affected by Cs+ and 4-aminopyridine. The ISAH was initially augmented and subsequently depressed by apamin (1-10 nM) and (+)-tubocurarine (100-600 microM). It is concluded that the ISAH in visceral primary neurones may be due to a long-lasting increase in K+ conductance caused by an increase in the concentration of intracellular Ca2+, resulting from Ca2+ entry during the depolarizing command pulse.
Morita
K
K
Department of Autonomic Physiology, Tokyo Medical and Dental University, Japan.
Katayama
Y
Y
D000818:Animals; D001030:Apamin / Q000494:pharmacology; D000001:Calcimycin / Q000494:pharmacology; D002118:Calcium / Q000502:physiology*; D002121:Calcium Channel Blockers / Q000494:pharmacology; D005260:Female; D008297:Male; D009475:Neurons, Afferent / Q000502:physiology*; D011817:Rabbits; D013237:Stereoisomerism; D019789:Tetraethylammonium; D013757:Tetraethylammonium Compounds / Q000494:pharmacology; D014403:Tubocurarine / Q000494:pharmacology; D014781:Viscera / Q000166:cytology / Q000502:physiology*
D002121:Calcium Channel Blockers; D013757:Tetraethylammonium Compounds; D001030:Apamin; D000001:Calcimycin; D019789:Tetraethylammonium; D002118:Calcium; D014403:Tubocurarine