Chronic nicotine alters nicotinic receptor-induced presynaptic Ca2+ responses in isolated nerve terminals.
作者： John J. Dougherty , Jianlin Wu , Tejal K. Mehta , Brett Brown , Robert A. Nichols
DOI: 10.1007/S11064-007-9557-9
关键词:
摘要: Brain nicotinic receptors display pronounced permeability for Ca2+ and localize to presynaptic nerve terminals, in addition postsynaptic sites. Chronic exposure nicotine has been shown alter brain receptor expression, but the functional consequences have not directly examined. Here, we used confocal imaging assess responses individual terminals from cortices of mice treated up 14 days with as compared vehicle-treated controls. treatment led substantially enhanced amplitudes acute application at concentrations 50 nM (2-fold) 500 (1.7-fold), microM. In addition, increased expression high-affinity on isolated was observed following chronic treatment, determined immunocytochemically pharmacologically. These findings suggest that may lead sensitivity select sites via up-regulation receptors.
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