Identification of ATP-sensitive K+ Conductances in Male Rat Major Pelvic Ganglion Neurons.
- Author:
Kyu Sang PARK
1
;
Seung Kyu CHA
;
Keon Il LEE
;
Jae Yeoul JUN
;
Seong Woo JEONG
;
In Deok KONG
;
Joong Woo LEE
Author Information
1. Department of Physiology, Yonsei University Wonju College of Medicine, Wonju, Korea. kong@wonju.yonsei.ac.kr
- Publication Type:Original Article
- Keywords:
ATP-sensitive K+ channel;
Major pelvic ganglia;
Phenotype-specific;
Metabolic inhibition
- MeSH:
Animals;
Anoxia;
Diazoxide;
Electron Transport;
Fires;
Ganglia;
Ganglion Cysts*;
Glyburide;
Humans;
Male*;
Membrane Potentials;
Membranes;
Neurons*;
Rats*
- From:The Korean Journal of Physiology and Pharmacology
2002;6(5):247-254
- CountryRepublic of Korea
- Language:English
-
Abstract:
Major pelvic ganglia (MPG) neurons are classified into sympathetic and parasympathetic neurons according to the electrophysiological properties; membrane capacitance (Cm), expression of T-type Ca2+ channels, and the firing patterns during depolarization. In the present study, function and molecular expression of ATP-sensitive K+ (K(ATP)) channels was investigated in MPG neurons of male rats. Only in parasympathetic MPG neurons showing phasic firing patterns, hyperpolarizing changes were elicited by the application of diazoxide, an activator of K(ATP) channels. Glibenclamide (10microM), a K(ATP) channel blocker, completely abolished the diazoxide-induced hyperpolarization. Diazoxide increased inward currents at high K+ (90 mM) external solution, which was also blocked by glibenclamide. The metabolic inhibition by the treatment with mitochondrial respiratory chain inhibitors (rotenone and antimycin) hyperpolarized the resting membrane potential of parasympathetic neurons, which was not observed in sympathetic neurons. The hyperpolarizing response to metabolic inhibition was partially blocked by glibenclamide. RT-PCR analysis revealed that MPG neurons mainly expressed the K(ATP) channel subunits of Kir6.2 and SUR1. Our results suggest that MPG neurons have K(ATP) channels, mainly formed by Kir6.2 and SUR1, with phenotype-specificity, and that the conductance through this channel in parasympathetic neurons may contribute to the changes in excitability during hypoxia and/or metabolic inhibition.
