Nicotinic receptor-mediated filtering of mitral cell responses to olfactory nerve inputs involves the α3β4 subtype.
Nicotinic receptor-mediated filtering of mitral cell responses to olfactory nerve inputs involves the α3β4 subtype.
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DOI：
10.1523/jneurosci.5024-11.2012
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发表时间：
2012-02-29
期刊：
影响因子：
--
通讯作者：
Vijayaraghavan S
中科院分区：
文献类型：
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作者：
D'Souza RD;Vijayaraghavan S
Acetylcholine plays a major role in the processing of sensory inputs. Cholinergic input to the mammalian olfactory bulb modulates odor discrimination and perceptual learning by mechanisms that are yet to be elucidated. We have used the mouse olfactory bulb in order to examine the role of nicotinic acetylcholine receptors (nAChRs) in regulating the responses of mitral cells (MCs), the output neurons of the olfactory bulb, to olfactory nerve input. We show that acetylcholine activates α3β4* nAChRs (* denotes possible presence of other subunits) on MCs leading to their excitation. Despite depolarizing MCs directly, the net effect of nAChR activation is to suppress olfactory nerve-evoked responses in these cells via activity-dependent, feedback GABAergic mechanisms. Our results indicate that nAChRs gate incoming olfactory nerve input wherein weak input stimuli are filtered out, while strong stimuli are transmitted via the MCs. Based on our observations, we provide a mechanistic model for the sharpening of mitral cell receptive fields by nAChRs, which could aid in odor discrimination and perceptual learning.
