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Dysfunction of M-channel enhances propagation of neuronal excitability in rat hippocampus monitored by multielectrode dish and microdialysis systems

Gang Zhu, Motohiro Okada, Takuya Murakami, Akihisa Kamata, Yuko Kawata,
Kazumaru Wada, Sunao Kaneko
Neuroscience Letters (2000) , 294 , 53-57

To explore the pathogenesis of benign familial neonatal convulsions (BFNC), we determined effects of KCNQ-related M-channels (KCNQ-channels) on hippocampal glutamate (Glu) and g-aminobutyric acid (GABA) releases using microdialysis, and propagation of evoked fiel-potentials (FP) using multielectrode (64-ch) dish system as two-dimensional monitoring. KCNQ channel inhibitor inhibitor, Dup996, enhanced hippocampal K+-evoked Glu and GABA releases without affecting basal releases of them. Dup996 unaffected FP-amplitude, but enhanced FP-propagation. The GABAA -receptor antagonist, bicuculline, enhanced the stimulatory effects of Dup996 on FP-propagation, however, this stimulatory effects of Dup996 were abolished by the a-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA)/glutamate-receptor antagonist, DNQX. These results suggest that the occurrence of BFNC cannot be produced by KCNQ-channel dysfunction alone, but by reciprocal action between impaired KCNQ-channel and other unknown elements (possibly dysfunction of inhibitory neurotransmission system).

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