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First published online on April 19, 2002.
 Copyright © 2002 by The Physiological Society
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Received February 3, 2002
Accepted after revision March 12, 2002

Pre- and postsynaptic ATP-sensitive potassium channels during metabolic inhibition of rat hippocampal CA1 neurons

Nozomu Matsumoto1, Sohtaro Komiyama2, and N. Akaike3*

1 Cellular and System Physiology, Graduate School of Medical Sciences, Kyushu University, and Department of Otorhinolaryngology, Faculty of Medicine, Kyushu University, Fukuoka 812-8582, Japan
2 Department of Otorhinolaryngology, Faculty of Medicine, Kyushu University, Fukuoka 812-8582, Japan
3 Cellular and System Physiology, Graduate School of Medical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan

* To whom correspondence should be addressed. E-mail: akaike{at}physiol2.med.kyushu-u. ac.jp.

Presynaptic and postsynaptic membrane activities during experimental metabolic inhibition were analysed in mechanically dissociated rat hippocampal neurons using nystatin-perforated and conventional whole-cell patch clamp recordings. NaCN, an inhibitor of mitochondrial ATP synthesis, induced an outward current across the postsynaptic soma membrane. This current was blocked by tolbutamide, a sulfonylurea, which blocks ATP-sensitive K+ (KATP) channels. The presynaptic effect of metabolic inhibitors such as NaCN, NaN3, or glucose-free solution was to increase the frequency of GABAergic miniature inhibitory postsynaptic currents (mIPSCs). Tolbutamide had no effect on this increase in mIPSC frequency induced by metabolic inhibition. Diazoxide, a KATP channel opener, evoked a similar somatic outward current in a dose-dependent manner. In addition, diazoxide decreased the frequency of mIPSCs in a dose-dependent fashion. Both these pre- and postsynaptic effects of diazoxide were reversed by tolbutamide, suggesting the existence of KATP channels on both pre- and postsynaptic membranes. These results confirm the presence of KATP channels on both the pre- and postsynaptic membranes but indicate that the channels have significantly different sensitivities to metabolic inhibition.




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