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Group 1 metabotropic glutamate receptor 5 is involved in synaptically-induced Ca2+-spikes and cell death in cultured rat hippocampal neurons
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Type
Academic journal
Author
양지선 (가톨릭대학교) Jeon Su Jeong (가톨릭대학교) Jang Hyun Jong (가톨릭대학교) Shin-Hee Yoon (가톨릭대학교)
Journal
The Korean Society Of Pharmacology The Korean Journal of Physiology & Pharmacology The Korean Journal of Physiology & Pharmacology 제26권 제6호 KCI Accredited Journals
Published
2022.11
Pages
531 - 540 (10page)
DOI
10.4196/kjpp.2022.26.6.531

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Group 1 metabotropic glutamate receptor 5 is involved in synaptically-induced Ca2+-spikes and cell death in cultured rat hippocampal neurons
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Research history (3)

2022

Group 1 metabotropic glutamate receptor 5 is involved in synaptically-induced Ca2+-spikes and cell death in cultured rat hippocampal neurons
Jeon Su Jeong ,  Jang Hyun Jong ,  Shin-Hee Yoon and others 0 The Korean Journal of Physiology & Pharmacology 2022.11 Academic journal

2018

Cyanidin-3-glucoside inhibits amyloid β25-35-induced neuronal cell death in cultured rat hippocampal neurons
,  Yoon Kee Dong ,  Shin-Hee Yoon and others 0 The Korean Journal of Physiology & Pharmacology 2018.11 Academic journal

2015

배양한 흰쥐 해마세포에서 칼슘이온 유도 미토콘드리아 탈분극과 활성산소종 생성감소를 통한 glutamate에 의한 아연 이온신호와 세포사멸에 대한 cyanidin-3-glucoside의 억제효과
양지선 신경생물학 2015.01 Thesis
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Abstract· Keywords

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Group 1 metabotropic glutamate receptors (mGluRs) can positively affect postsynaptic neuronal excitability and epileptogenesis. The objective of the present study was to determine whether group 1 mGluRs might be involved in synapticallyinduced intracellular free Ca2+ concentration ([Ca2+]i) spikes and neuronal cell death induced by 0.1 mM Mg2+ and 10 µM glycine in cultured rat hippocampal neurons from embryonic day 17 fetal Sprague–Dawley rats using imaging methods for Ca2+ and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assays for cell survival. Reduction of extracellular Mg2+ concentration ([Mg2+]o) to 0.1 mM induced repetitive [Ca2+]i spikes within 30 sec at day 11.5. The mGluR5 antagonist 6-Methyl- 2-(phenylethynyl) pyridine (MPEP) almost completely inhibited the [Ca2+]i spikes, but the mGluR1 antagonist LY367385 did not. The group 1 mGluRs agonist, 3,5-dihydroxyphenylglycine (DHPG), significantly increased the [Ca2+]i spikes. The phospholipase C inhibitor U73122 significantly inhibited the [Ca2+]i spikes in the absence or presence of DHPG. The IP3 receptor antagonist 2-aminoethoxydiphenyl borate or the ryanodine receptor antagonist 8-(diethylamino)octyl 3,4,5-trimethoxybenzoate also significantly inhibited the [Ca2+]i spikes in the absence or presence of DHPG. The TRPC channel inhibitors SKF96365 and flufenamic acid significantly inhibited the [Ca2+]i spikes in the absence or presence of DHPG. The mGluR5 antagonist MPEP significantly increased the neuronal cell survival, but mGluR1 antagonist LY367385 did not. These results suggest a possibility that mGluR5 is involved in synapticallyinduced [Ca2+]i spikes and neuronal cell death in cultured rat hippocampal neurons by releasing Ca2+ from IP3 and ryanodine-sensitive intracellular stores and activating TRPC channels. INTRODUCTION Glutamate can activate non-N-methyl-D-aspartate (non- NMDA) receptors, leading to depolarize membranes in neurons. This depolarization can induce Ca2+ influx from the extracellular space by decreasing Mg2+ block of N-methyl-D-aspartate (NMDA) receptors and activating voltage-gated Ca2+ channels. Glutamate can also induce the release of Ca2+ from intracellular stores throu
#Calcium spike #Hippocampus #IP3 receptor #Magnesium #Metabotropic glutamate receptor

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