ArticleNeurobiology of learning and memory2022
Nicotine-mediated activation of α2 nAChR-expressing OLM cells in developing mouse brains disrupts OLM cell-mediated control of LTP in adolescence.
Article in Neurobiology of learning and memory, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Early postnatal nicotine exposure, a rodent model of smoking during pregnancy, affects hippocampal synaptic plasticity and memory. Here, we investigated the role of α2 nAChR-expressing OLM (α2-OLM) cells in LTP in unexposed and postnatal nicotine-exposed mice. We found that reduced α2 nAChR-dependent activation of OLM cells in α2 heterozygous knockout mice prevented LTP, whereas enhanced α2 nAChR-dependent activation of OLM cells in heterozygous knockin mice expressing hypersensitive α2 nAChRs facilitated LTP. Both optogenetic and chemogenetic activation of α2-OLM cells facilitated LTP as nicotine did. However, in postnatal nicotine-exposed mice, expressing chemogenetic hM3Dq receptors in α2-OLM cells, LTP was facilitated and both nicotinic and chemogenetic activation of α2-OLM cells prevented rather than facilitated LTP. These results demonstrate a critical role of α2-OLM cell activation in LTP as well as altered α2-OLM cell function in postnatal nicotine-exposed mice. To determine whether nicotine-mediated α2 nAChR activation in developing brains causes facilitated LTP and altered nicotinic modulation of LTP in adolescence, we used homozygous knockin mice expressing hypersensitive α2 nAChRs as a way to selectively activate α2-OLM cells. In the knockin mice, postnatal exposure to a low dose of nicotine, which had no effect on LTP in wild-type mice, is sufficient to cause facilitated LTP and altered nicotinic modulation of LTP as found in wild-type mice exposed to a higher dose of nicotine. Thus, the nicotine-mediated activation of α2 nAChRs on OLM cells in developing brains disrupts the α2-OLM cell-mediated control of LTP in adolescence that might be linked to impaired memory.
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