HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (6) Citing Articles via Google Scholar Google Scholar Articles by Ji, W. Articles by Gao, E. Search for Related Content PubMed PubMed Citation Articles by Ji, W. Articles by Gao, E.

Effects of Agonists and Antagonists of NMDA and ACh Receptors on Plasticity of Bat Auditory System Elicited by Fear Conditioning

Department of Biology, Washington University, St. Louis, Missouri

Submitted 31 January 2005; accepted in final form 5 May 2005

In big brown bats, tone-specific plastic changes [best frequency (BF) shifts] of cortical and collicular neurons can be evoked by auditory fear conditioning, repetitive acoustic stimuli or cortical electric stimulation. It has been shown that acetylcholine (ACh) plays an important role in evoking large long-term cortical BF shifts. However, the role of N-methyl-D-aspartate (NMDA) receptors in evoking BF shifts has not yet been studied. We found 1) NMDA applied to the auditory cortex (AC) or inferior colliculus (IC) augmented the auditory responses, as ACh did, whereas 2-amino-5-phosphovalerate (APV), an antagonist of NMDA receptors, reduced the auditory responses, as atropine did; 2) although any of these four drugs did not evoke BF shifts, they influenced the development of the long-term cortical and short-term collicular BF shifts elicited by conditioning; 3) like ACh, NMDA augmented the cortical and collicular BF shifts regardless of whether it was applied to the AC or IC; 4) endogenous ACh of the AC and IC is necessary to produce the long-term cortical and short-term collicular BF shifts; 5) blockade of collicular NMDA receptors by APV abolished the development of the collicular BF shift and made the cortical BF shift small and short-term; 6) blockade of cortical NMDA receptors by APV reduced the cortical and collicular BF shifts and made the cortical BF shift short-term; and 7) conditioning with NMDA + atropine applied to the AC evoked the small, short-term cortical BF shift, whereas conditioning with APV + ACh applied to the AC evoked the small, but long-term cortical BF shift.

This article has been cited by other articles:

				N. M. Weinberger Retuning the brain by learning, literature, and logic: Reply to Suga Learn. Mem., March 28, 2008; 15(4): 202 - 207. [Full Text] [PDF]

				N. Suga The neural circuit for tone-specific plasticity in the auditory system elicited by conditioning Learn. Mem., March 20, 2008; 15(4): 198 - 201. [Full Text] [PDF]

				G. Soto, N. Kopell, and K. Sen Network Architecture, Receptive Fields, and Neuromodulation: Computational and Functional Implications of Cholinergic Modulation in Primary Auditory Cortex J Neurophysiol, December 1, 2006; 96(6): 2972 - 2983. [Abstract] [Full Text] [PDF]

				Y. Zhang, S. E. Hamilton, N. M. Nathanson, and J. Yan Decreased Input-Specific Plasticity of the Auditory Cortex in Mice Lacking M1 Muscarinic Acetylcholine Receptors Cereb Cortex, September 1, 2006; 16(9): 1258 - 1265. [Abstract] [Full Text] [PDF]