Watanabe K, Onozuka M
Department of Physiology, Gifu University School of Medicine, Japan.
Brain Res. 1994 Aug 22;654(2):352-6. doi: 10.1016/0006-8993(94)90500-2.
The inhibitory action of glutamate (Glu) was examined in identified Euhadra neurons, using the voltage-clamp method in combination with the pressure injection technique. Glu elicited a slow outward K+ current (Glu current) whose amplitude was dose-dependent. This current was inhibited by exogenous Ca2+/calmodulin-dependent protein kinase II (CaMKII) and is enhanced by a specific CaMKII inhibitor. However, no significant changes in the Glu current were observed when the catalytic subunit of protein kinase A (PKA) or the protein kinase C (PKC) fragment (530-558) was intracellularly applied; or using a PKA inhibitor or a PKC inhibitor. Neither the antagonists of the Glu receptor, D-2-amino-5-monophosphonovalerate, 6-cyano-7-nitroquinoxaline-2,3 dione and kynurenic acid, nor the G protein blockers, pertussis toxin and chorela toxin, had any significant effect on the Glu current. These results indicate that Glu opens the CaMKII-suppressing K+ channels, suggesting a novel Glu-induced inhibitory mechanism.
