کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8479172 | 1551292 | 2015 | 7 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
The effects of JM-20 on the glutamatergic system in synaptic vesicles, synaptosomes and neural cells cultured from rat brain
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کلمات کلیدی
AMPAΔpHJM-20VGLUTsN-methyl-d-aspartateNMDAEAATsDMEMHBSSEGTAF-ATPaseGFAPV-ATPaseDMSO - DMSODulbecco's modified Eagle's medium - Medal of Eagle اصلاح شده DulbeccoAstrocytes - آستروسیتVesicular glutamate transporters - حمل و نقل گلوتامات VesicularDIV - دیوDimethyl sulfoxide - دیمتیل سولفواکسیدdays in vitro - روز in vitroglutamatergic system - سیستم glutamatergicSynaptosomes - سیناپتوزوم هاinorganic phosphate - فسفات معدنیHank's balanced salt solution - محلول نمک متعادل هانکNeurons - نورون ها،یاخته های عصبیsynaptic vesicle - واژینال سیناپسیGlial fibrillary acidic protein - پروتئین اسیدی فیبریلاسیون گلایالhigh-performance liquid chromatography - کروماتوگرافی مایعی کاراHPLC - کروماتوگرافی مایعی کارا
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
بیولوژی سلول
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چکیده انگلیسی
JM-20 (3-ethoxycarbonyl-2-methyl-4-(2-nitrophenyl)-4,11-dihydro-1H-pyrido[2,3-b][1,5]benzodiazepine) is a novel benzodiazepine dihydropyridine hybrid molecule, which has been shown to be a neuroprotective agent in brain disorders involving glutamate receptors. However, the effect of JM-20 on the functionality of the glutamatergic system has not been investigated. In this study, by using different in vitro preparations, we investigated the effects of JM-20 on (i) rat brain synaptic vesicles (L-[3H]-glutamate uptake, proton gradient built-up and bafilomycin-sensitive H+-ATPase activity), (ii) rat brain synaptosomes (glutamate release) and (iii) primary cultures of rat cortical neurons, astrocytes and astrocyte-neuron co-cultures (L-[3H]-glutamate uptake and glutamate release). We observed here that JM-20 impairs H+-ATPase activity and consequently reduces vesicular glutamate uptake. This molecule also inhibits glutamate release from brain synaptosomes and markedly increases glutamate uptake in astrocytes alone, and co-cultured neurons and astrocytes. The impairment of vesicular glutamate uptake by inhibition of the H+-ATPase caused by JM-20 could decrease the amount of the transmitter stored in synaptic vesicles, increase the cytosolic levels of glutamate, and will thus down-regulate neurotransmitter release. Together, these results contribute to explain the anti-excitotoxic effect of JM-20 and its strong neuroprotective effect observed in different in vitro and in vivo models of brain ischemia.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neurochemistry International - Volume 81, February 2015, Pages 41-47
Journal: Neurochemistry International - Volume 81, February 2015, Pages 41-47
نویسندگان
Yanier Nuñez-Figueredo, Gilberto L. Pardo Andreu, Samanta Oliveira Loureiro, Marcelo Ganzella, Jeney RamÃrez-Sánchez, Estael Ochoa-RodrÃguez, Yamila Verdecia-Reyes, René Delgado-Hernández, Diogo O. Souza,