Effects of zonisamide on K+ and Ca2+ evoked release of monoamine as well as K+ evoked intracellular Ca2+ mobilization in rat hippocampus

To clarify the effects of zonisamide (ZNS) on neurotransmission and intracellular Ca2+ mobilization, both Ca2+ and K+ evoked hippocampal releases of dopamine (DA) and serotonin (5-HT) were determined by in vivo microdialysis, and K+ (25 and 50 mM) evoked elevation of intracellular Ca2+ level was det...

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Published in:Epilepsy research 1999-07, Vol.35 (3), p.173-182
Main Authors: KAWATA, Y, OKADA, M, MURAKAMI, T, MIZUNO, K, WADA, K, KONDO, T, KANEKO, S
Format: Article
Language:English
Subjects:
Animals
Anticonvulsants - pharmacology
Anticonvulsants. Antiepileptics. Antiparkinson agents
Biogenic Monoamines - metabolism
Biological and medical sciences
Calcium - metabolism
Calcium - pharmacology
Chromatography, High Pressure Liquid
Dopamine - metabolism
Hippocampus - drug effects
Hippocampus - metabolism
Image Processing, Computer-Assisted
Isoxazoles - pharmacology
Male
Medical sciences
Microdialysis
Neuropharmacology
Pharmacology. Drug treatments
Potassium - pharmacology
Rats
Rats, Wistar
Serotonin - metabolism
Synaptic Transmission - physiology
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Summary:To clarify the effects of zonisamide (ZNS) on neurotransmission and intracellular Ca2+ mobilization, both Ca2+ and K+ evoked hippocampal releases of dopamine (DA) and serotonin (5-HT) were determined by in vivo microdialysis, and K+ (25 and 50 mM) evoked elevation of intracellular Ca2+ level was determined by fluorescence microscopy in vitro. Therapeutic concentrations of ZNS had different effects on Ca2+ and K+ evoked release of monoamine. ZNS stimulated Ca2+ evoked monoamine release, while ZNS inhibited K+ evoked monoamine release. ZNS inhibited K+ evoked elevation of hippocampal intracellular Ca2+ levels in a concentration dependent manner. These results suggest that ZNS inhibits the depolarization induced by neuronal excitation, whereas ZNS might enhance the N-type Ca2+ channel activity or N-type Ca2+ channel related exocytosis mechanisms.
ISSN:0920-1211
1872-6844
DOI:10.1016/s0920-1211(99)00010-8