Curcumin inhibits glutamate release from rat prefrontal nerve endings by affecting vesicle mobilization |
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Authors: | Tzu Yu Lin Cheng Wei Lu Shu Kuei Huang Su Jane Wang |
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Affiliation: | Department of Anesthesiology, Far-Eastern Memorial Hospital, Pan-Chiao District, New Taipei City 22060, Taiwan; E-Mails: drlin1971@gmail.com (T.Y.L.); drluchengwei@gmail.com (C.W.L.); nskh9450n@yahoo.com.tw (S.K.H.). |
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Abstract: | Curcumin, one of the major constituents of Curcuma longa, has been shown to inhibit depolarization-evoked glutamate release from rat prefrontocortical nerve terminals by reducing voltage-dependent Ca(2+) entry. This study showed that curcumin inhibited ionomycin-induced glutamate release and KCl-evoked FM1-43 release, suggesting that some steps after Ca(2+) entry are regulated by curcumin. Furthermore, disrupting the cytoskeleton organization using cytochalasin D abolished the inhibitory action of curcumin on ionomycin-induced glutamate release. Mitogen-activated protein kinase kinase (MEK) inhibition also prevented the inhibitory effect of curcumin on ionomycin-induced glutamate release. Western blot analyses showed that curcumin decreased the ionomycin-induced phosphorylation of extracellular signal-regulated kinase 1 and 2 (ERK1/2) and synaptic vesicle-associated protein synapsin I, the main presynaptic target of ERK. These results show that curcumin-mediated inhibition of glutamate release involves modulating downstream events by controlling synaptic vesicle recruitment and exocytosis, possibly through a decrease of MAPK/ERK activation and synapsin I phosphorylation, thereby decreasing synaptic vesicle availability for exocytosis. |
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Keywords: | curcumin glutamate exocytotic machinery ERK synapsin I prefrontocortical nerve terminals |
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