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A novel glutamate-mediated inhibitory mechanism linked with Ca2+/calmodulin-dependent protein kinase II in identifiedEuhadra neurons

✍ Scribed by Watanabe, Kazuko ;Yamamoto, Tetsu ;Ozono, Satoru ;Nagasaki, Sachio ;Onozuka, Minoru


Publisher
John Wiley and Sons
Year
1997
Tongue
English
Weight
169 KB
Volume
32
Category
Article
ISSN
0022-3034

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✦ Synopsis


The underlying mechanism(s) of manner, while intracellularly injected CaM-KII the glutamate (Glu)-induced membrane hyperpolarsuppresses the current. The potent protein kinase A izing response in identified Euhadra neurons was investigated using the voltage-clamp technique, pressure inhibitors, H-8 (N-[2-(methylamino)ethyl]-5-isoquiinjection method, and pharmacologic agents. Under nolinesulfonamide dihydrochloride) and H-89 (N-[2voltage-clamp conditions, bath-applied Glu elicits a (p -bromocinnamylamino)ethyl] -5 -isoquinolinesulslow outward potassium current (Glu current) acfonamide) or the specific protein kinase C inhibitors companied by an increase in membrane conductance staurosporine and K-252b had no effect on the Glu whose amplitude is dose dependent. Of the agonists current. These results suggest the presence of a novel tested, the Glu current was mimicked only by quisquasubtype of Glu receptor in Euhadra neurons, which late (QA); its potency was approximately 10 times may be coupled to the activation of potassium changreater than that of Glu. Typical antagonists for the nels normally suppressed by CaM-KII. ᭧ 1997 John ionotropic type of Glu receptors and G protein inhibi-Wiley & Sons, Inc. J Neurobiol 32: 139-149, 1997 tors do not block this current. The Glu current is Keywords: glutamate; membrane hyperpolarization; markedly enhanced by a specific inhibitor of Ca 2/ / potassium channels; Ca 2/ /CaM-dependent protein calmodulin-dependent protein kinase II (CaM-KII), kinase II; mollusan neurons KN-62 (1-[N,O-bis(1,5-isoquinolinesulfonyl)-N-methyl-