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ORIGINAL ARTICLE
Year : 2021  |  Volume : 64  |  Issue : 6  |  Page : 266-273

Nicotinamide adenine dinucleotide promotes synaptic plasticity gene expression through regulation N-methyl-D-aspartate receptor/Ca2+/Erk1/2 pathway


1 Department of Anatomy, School of Basic Medical Sciences, Shandong University, Jinan, Shandong, China
2 Department of Neurosurgery, The Third Affiliated Hospital of Shandong First Medical University, Affiliated Hospital of Shandong Academy of Medical Sciences, Jinan, Shandong, China
3 Morphological Experimental Center, School of Basic Medical Sciences, Shandong University, Jinan, Shandong, China
4 Department of Uitrasound, Second Hospital of Shandong University, Jinan, Shandong, China

Correspondence Address:
Dr. Jin-Hao Sun
Department of Anatomy and Neurobiology, School of Basic Medicine, Shandong University, Jinan 250012, Shandong
China
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/cjp.cjp_42_21

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Nicotinamide adenine dinucleotide (NADH) has been reported to regulate synaptic plasticity recently, while its role in this process remains unclear. To explore the contribution and the underlying mechanisms of NADH regulating synaptic plasticity, here, we examined NADH's effect on immediate-early response genes (IEGs) expressions, including C-Fos and Arc in primary cultured cortical neurons and the frontal cortex of mouse brain. Our results showed that NADH promoted IEGs expression and that the C-Fos and Arc levels are increased in primary cultured cortical neurons, which is almost completely blocked by N-methyl-D-aspartate receptor (NMDAR) inhibitor, MK-801. Moreover, NADH significantly increased intracellular Ca2+ levels and the phosphorylation of Erk1/2, a downstream molecule of the NMDAR. Furthermore, NADH also significantly increased IEGs expression in vivo, accompanied by the changes of Ca2+ in neurons and activation of excitatory neurons in the mouse frontal cortex. In conclusion, this study indicates that NADH can promote the expression of synaptic plasticity-related IEGs through the NMDAR/Ca2+/Erk1/2 pathway, which provides a new way to understand the regulatory role of NADH in synaptic plasticity.


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