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KMID : 1161920180150020067
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Journal of Medicine and Life Science
2018 Volume.15 No. 2 p.67 ~ p.71
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Endogenous glutamate enhances survival rates of neurons via activating mitochondrial signalings in hippocampal neuron
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Noh Jin-Woo
Kim Hye-Ji
Eun Su-Yong
Kang Moon-Suk
Jung Sung-Cherl
Yang Yoon-Sil
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Abstract
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Neuronal excitotoxicity induces mitochondrial dysfunction and the release of proapoptotic proteins. Excitotoxicity, the process by which the overactivation of excitatory neurotransmitter receptors leads to neuronal cell death. Neuronal death by excitotoxicity was related to neuronal degenerative disorders and hypoxia, results from excessive exposure to excitatory neurotransmitters, such as glutamate. Glutamate acts at NMDA receptors in cultured neurons to increase the intracellular free calcium concentration. Therefore endogenous glutamate may be a key factor to regulate neuronal cell death via activating Ca2+ signaling. For this issue, we tested some conditions to alter intracellular Ca2+ level in dissociated hippocampal neurons of rats. Cultured hippocampal neuron were treated by KCl (20 mM), CaCl₂3.8 mM and glutamate (5 μM) for 24hrs. Interestingly, The Optical Density of hippocampal neurons was increased by high KCl application in MTT assay data. This enhanced response by high KCl was dependent on synaptic Ca2+ influx but not on intracellular Ca2+ level. However, the number of neurons seemed to be not changed in hoechst33342 staining data. These results suggest that enhancement of synaptic activity plays a key role to increase mitochondrial signaling in hippocampal neurons.
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KEYWORD
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Glutamate, Excitotoxicity, Neuronal death, NMDA, Ca2+, KCl, Mitochondria
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