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Allicin Inhibits Glutamate Release from Rat Cerebral Cortex Nerve Terminals Through Suppressing Ca2+ Influx and Protein Kinase C Activity

Journal of Medicinal Food 2019년 22권 7호 p.696 ~ 702
Lu Cheng-Wei, Hung Chi-Feng, Lin Tzu-Yu, Hsieh Ting Yang, Wang Su Jane,
소속 상세정보
 ( Lu Cheng-Wei ) - Far-Eastern Memorial Hospital Department of Anesthesiology
 ( Hung Chi-Feng ) - Fu Jen Catholic University School of Medicine
 ( Lin Tzu-Yu ) - Far-Eastern Memorial Hospital Department of Anesthesiology
 ( Hsieh Ting Yang ) - Fu Jen Catholic University P.H.D. Program in Nutrition and Food Science
 ( Wang Su Jane ) - Fu Jen Catholic University School of Medicine

Abstract


Evidence indicates that indirect inhibitory regulation of glutamatergic transmission, via reducing glutamate release, may induce neuroprotection. The present work was designed to examine whether allicin, a major component of garlic with neuroprotective effects, affected the release of glutamate evoked by 4-aminopyridine in rat cerebrocortical nerve terminals (synaptosomes). Allicin caused a potent inhibition on the release of glutamate evoked by 4-aminopyridine, and this inhibitory effect was abolished in the presence of Ca2+-free medium and vesicular transporter inhibitor. Allicin decreased the 4-aminopyridine-evoked elevation of intrasynaptosomal Ca2+ levels, but had no effect on the synaptosomal plasma membrane potential. The allicin-mediated inhibition of glutamate release was prevented by the N- and P/Q-type channel blocker and the protein kinase C (PKC) inhibitor, but was not affected by the intracellular Ca2+-release inhibitors, mitogen-activated protein kinase inhibitor, and protein kinase A inhibitor. Western blotting data also showed that allicin significantly reduced the phosphorylation of PKC. Together, these data indicate that in rat cerebrocortical nerve terminals, allicin depresses glutamate release and appears to decrease N- and P/Q-type Ca2+ channel and PKC activity.

키워드

allicin; cerebrocortical synaptosomes; glutamate release; presynaptic Ca2+ channels; protein kinase C

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