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dc.contributor.authorChan W.
dc.contributor.authorSingh S.
dc.contributor.authorKeshav T.
dc.contributor.authorDewan R.
dc.contributor.authorEberly C.
dc.contributor.authorMaurer R.
dc.contributor.authorNunez-Parra A.
dc.contributor.authorAraneda R.C.
dc.date.accessioned2020-09-02T22:14:49Z
dc.date.available2020-09-02T22:14:49Z
dc.date.issued2017
dc.identifier10.3389/fnsyn.2017.00004
dc.identifier.citation9, FEB, -
dc.identifier.issn16633563
dc.identifier.urihttps://hdl.handle.net/20.500.12728/4003
dc.descriptionThe cholinergic system has extensive projections to the olfactory bulb (OB) where it produces a state-dependent regulation of sensory gating. Previous work has shown a prominent role of muscarinic acetylcholine (ACh) receptors (mAChRs) in regulating the excitability of OB neurons, in particular the M1 receptor. Here, we examined the contribution of M1 and M3 mAChR subtypes to olfactory processing using mice with a genetic deletion of these receptors, the M1-/- and the M1/M3-/- knockout (KO) mice. Genetic ablation of the M1 and M3 mAChRs resulted in a significant deficit in odor discrimination of closely related molecules, including stereoisomers. However, the discrimination of dissimilar molecules, social odors (e.g., urine) and novel object recognition was not affected. In addition the KO mice showed impaired learning in an associative odor-learning task, learning to discriminate odors at a slower rate, indicating that both short and long-term memory is disrupted by mAChR dysfunction. Interestingly, the KO mice exhibited decreased olfactory neurogenesis at younger ages, a deficit that was not maintained in older animals. In older animals, the olfactory deficit could be restored by increasing the number of new born neurons integrated into the OB after exposing them to an olfactory enriched environment, suggesting that muscarinic modulation and adult neurogenesis could be two different mechanism used by the olfactory system to improve olfactory processing. © 2017 Chan, Singh, Keshav, Dewan, Eberly, Maurer, Nunez-Parra and Araneda.
dc.language.isoen
dc.publisherFrontiers Research Foundation
dc.subjectAdult neurogenesis
dc.subjectGranule cell
dc.subjectInhibition
dc.subjectOlfactory
dc.subjectOlfactory discrimination
dc.subjectmuscarinic M1 receptor
dc.subjectmuscarinic M3 receptor
dc.subjectage
dc.subjectanimal cell
dc.subjectanimal experiment
dc.subjectanimal tissue
dc.subjectArticle
dc.subjectassociative learning test
dc.subjectcontrolled study
dc.subjectdiscrimination learning
dc.subjectfemale
dc.subjectgene deletion
dc.subjecthabituation
dc.subjectknockout mouse
dc.subjectlong term memory
dc.subjectmale
dc.subjectmouse
dc.subjectnerve cell differentiation
dc.subjectnonhuman
dc.subjectnovel object recognition test
dc.subjectolfactory bulb
dc.subjectolfactory discrimination
dc.subjectshort term memory
dc.subjectstimulus response
dc.subjectvisual discrimination
dc.subjectwild type
dc.titleMice lacking M1 and M3 muscarinic acetylcholine receptors have impaired odor discrimination and learning
dc.typeArticle


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