Identification of ATP-sensitive K⁢ Conductances in Male Rat Major Pelvic Ganglion Neurons

• 영문명: Identification of ATP-sensitive K^⁢ Conductances in Male Rat Major Pelvic Ganglion Neurons
• 발행기관: 대한생리학회-대한약리학회
• 저자명: Kyu-Sang Park Seung-Kyu Cha Keon-Il Lee Jae Yeoul Jun Seong-Woo Jeong In Deok Kong Joong Woo Lee
• 간행물 정보: 『The Korean Journal of Physiology & Pharmacology』제6권 제5호, 247~254쪽, 전체 8쪽
• 주제분류: 의약학 > 의학일반
• 파일형태: PDF
• 발행일자: 2002.01.01

영문 초록

Major pelvic ganglia (MPG) neurons are classified into sympathetic and parasympathetic neurons according to the electrophysiological properties; membrane capacitance (Cm), expression of T-type Ca^2⁢ 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 (10μM), 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.

키워드

ATP-sensitive K^⁢ channel Major pelvic ganglia Phenotype-specific Metabolic inhibition