Postnatal administration of memantine rescues TNF-α-induced decreasedhippocampal precursor proliferation
Postnatal administration of memantine rescues TNF-α-induced decreasedhippocampal precursor proliferation
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DOI：
10.1016/j.neulet.2017.10.022
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通讯作者：
何谐
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作者：
何谐
Pro-inflammatory cytokine exposure in early postnatal life triggers clear neurotoxic effects on the developing.hippocampus. Tumor necrosis factor alpha (TNF-α) is one of the inflammatory mediators and is a potent inhibitor of neurogenesis. Memantine (MEM) is an uncompetitive N-methyl-D-aspartate (NMDA) receptor antagonist that has been demonstrated to increase the proliferation of hippocampal progenitor cells. However, the.effects of MEM on TNF-α-mediated impairment of hippocampal precursor proliferation remain unclear. In this.study, mice were exposed to TNF-α and later treated with MEM to evaluate its protective effects on TNF-α-.mediated toxicity during hippocampal development. The results indicated that brief exposure to TNF-α on.postnatal days 3 and 5 resulted in a significant impairment of hippocampal precursor proliferation and a.depletion of hippocampal neural precursor cells (NPCs). This effect was attenuated by MEM treatment. We.further confirmed that MEM treatment reversed the TNF-α-induced microglia activation and up-regulation of.hippocampal NF-κB, MCP-1 and IL-6 mRNA levels, which may be related to the proliferation and maintenance of.NPCs. Overall, our results suggest that MEM treatment protects against TNF-α-induced repression of hippocampal precursor proliferation in postnatal mice by partially attenuating neuroinflammatory responses.
