Skip Navigation



Cerebral Cortex Advance Access published online on November 16, 2005
Cerebral Cortex, doi:10.1093/cercor/bhj067
This Article
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
16/9/1258    most recent
bhj067v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Zhang, Y.
Right arrow Articles by Yan, J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Zhang, Y.
Right arrow Articles by Yan, J.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Author 2005. Published by Oxford University Press. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org

Article

Decreased Input-Specific Plasticity of the Auditory Cortex in Mice Lacking M1 Muscarinic Acetylcholine Receptors

Yunfeng Zhang 1, Susan E. Hamilton 2, Neil M. Nathanson 2, and Jun Yan 1 *

1 Department of Physiology, Hotchkiss Brain Institute, University of Calgary Faculty of Medicine, Calgary, Alberta T2N 4N1, Canada
2 Department of Pharmacology, University of Washington School of Medicine, Seattle, WA 98195-7750, USA

* To whom correspondence should be addressed.
Jun Yan, E-mail: juyan{at}ucalgary.ca


  Abstract

Muscarinic acetylcholine receptors are extensively involved in cortical cognition and learning-induced or experience-dependent cortical plasticity. The most abundant muscarinic receptor subtype in the cerebral cortex is the M1 receptor, but little is known about its contribution to experience-dependent plasticity of the adult auditory cortex. We have examined the role of the M1 receptor in experience-dependent plasticity of the auditory cortex in mice lacking the M1 (chrm1) gene. We show here that electrical stimulation of the basal forebrain, a major source of cortical cholinergic inputs, facilitated the auditory responses of cortical neurons in both wild types and M1 mutants. The basal forebrain stimulation alone caused change in the best frequencies of cortical neurons that were significantly greater in M1 mutants. When animals received the paired stimuli of electrical stimulation of the basal forebrain and tone, the frequency tuning of cortical neurons systematically shifted toward the frequency of the paired tone in both wild types and M1 mutants. However, the shift range in M1 mutants was much smaller than that in wild-type mice. Our data suggest that the M1 receptor is important for the experience-dependent plasticity of the auditory cortex.

Keywords: auditory cortex; basal forebrain; cholinergic; cortical plasticity; frequency tuning; muscarinic acetylcholine receptor.
Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 J. Neurosci.Home page
F. Luo, Q. Wang, A. Kashani, and J. Yan
Corticofugal Modulation of Initial Sound Processing in the Brain
J. Neurosci., November 5, 2008; 28(45): 11615 - 11621.
[Abstract] [Full Text] [PDF]

Home page
 Cereb CortexHome page
Y. Zhang and J. Yan
Corticothalamic Feedback for Sound-Specific Plasticity of Auditory Thalamic Neurons Elicited by Tones Paired with Basal Forebrain Stimulation
Cereb Cortex, July 1, 2008; 18(7): 1521 - 1528.
[Abstract] [Full Text] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.