کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2201920 1100049 2008 11 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Facilitatory effect of glutamate exocytosis from rat cerebrocortical nerve terminals by α-tocopherol, a major vitamin E component
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی بیولوژی سلول
پیش نمایش صفحه اول مقاله
Facilitatory effect of glutamate exocytosis from rat cerebrocortical nerve terminals by α-tocopherol, a major vitamin E component
چکیده انگلیسی

The effect of α-tocopherol, the major vitamin E component, on the release of endogenous glutamate has been investigated using rat cerebrocortical nerve terminals. Results showed that α-tocopherol facilitated the Ca2+-dependent but not the Ca2+-independent glutamate release evoked by 4-aminopyridine (4AP). This release facilitation was insensitive to glutamate transporter inhibitor l-trans-PDC or dl-TBOA, and blocked by the exocytotic neurotransmitter release inhibitor tetanus neurotoxin, indicating that α-tocopherol affects specifically the physiological exocytotic vesicular release without affecting the non-vesicular release. Facilitation of glutamate exocytosis by α-tocopherol was not due to its increasing synaptosomal excitability, because α-tocopherol did not alter the 4AP-evoked depolarization of the synaptosomal plasma membrane potential. Rather, examination of the effect of α-tocopherol on cytoplasmic free Ca2+ concentration revealed that the facilitation of glutamate release could be attributed to an increase in voltage-dependent Ca2+ influx. Consistent with this, the α-tocopherol-mediated facilitation of glutamate release was significantly reduced in synaptosomes pretreated with ω-CgTX MVIIC, a wide spectrum blocker of N- and P/Q-type Ca2+ channels. In addition, α-tocopherol modulation of glutamate release appeared to involve a protein kinase C (PKC) signalling cascade, insofar as pretreatment of synaptosomes with the PKC inhibitor GF109203X effectively suppressed the facilitatory effect of α-tocopherol on 4AP- or ionomycin-evoked glutamate release. Furthermore, α-tocopherol increased the phosphorylation of MARCKS, the major presynapic substrate for PKC, and this effect was also significantly attenuated by PKC inhibition. Together, these results suggest that α-tocopherol exerts an increase in PKC activation, which subsequently enhances voltage-dependent Ca2+ influx and vesicular release machinery to cause an increase in evoked glutamate release from rat cerebrocortical glutamatergic terminals. This finding might provide important information regarding to the action of vitamin E in the central nervous system.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neurochemistry International - Volume 52, Issue 6, May 2008, Pages 979–989
نویسندگان
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