Differential expression of glycine receptor subunits in the rat basolateral and central amygdala

Delaney, A. J., Esmaeili, A., Sedlak, Petra L., Lynch, J. W. and Sah, P. (2010) Differential expression of glycine receptor subunits in the rat basolateral and central amygdala. Neuroscience Letters, 469 2: 237-242. doi:10.1016/j.neulet.2009.12.003


Author Delaney, A. J.
Esmaeili, A.
Sedlak, Petra L.
Lynch, J. W.
Sah, P.
Title Differential expression of glycine receptor subunits in the rat basolateral and central amygdala
Journal name Neuroscience Letters   Check publisher's open access policy
ISSN 0304-3940
1872-7972
0167-6253
Publication date 2010-01-22
Year available 2009
Sub-type Article (original research)
DOI 10.1016/j.neulet.2009.12.003
Open Access Status DOI
Volume 469
Issue 2
Start page 237
End page 242
Total pages 6
Editor S. G. Waxman
Place of publication Amsterdam, The Netherlands
Publisher Elsevier/North-Holland
Language eng
Subject C1
1109 Neurosciences
920111 Nervous System and Disorders
Abstract The amygdalar complex is a limbic structure that plays a key role in emotional processing and fear conditioning. Although inhibitory transmission in the amygdala is predominately GABA-ergic, neurons of the amygdala are also known to express glycine receptors. The subtype and function of these glycine receptors within the synaptic circuits of the amygdala are unknown. In this study, we have investigated the relative expression of the four major glycine receptor subunits (alpha 1-3 and beta) in the rat basolateral (BLA) and central amygdala (CeA), using real-time PCR and protein biochemistry. We demonstrate that alpha 1, alpha 2, alpha 3, and beta subunits are all expressed in the BLA and CeA with alpha 2 being the predominant alpha-subunit in both nuclei. Electrophysiological recordings from BLA and CeA neurons in acute brain slices indicated that differences in relative expression of these subunits were correlated with the pharmacological properties of native glycine receptors expressed on these neurons. We conclude that glycine receptors assembled in BLA neurons are largely alpha 1 beta-containing heteromultimers whereas receptors assembled in neurons of the central amygdala are primarily alpha 2 beta-, alpha 3 beta- or alpha 1 beta-containing heteromultimers, with a minor component of alpha 2 or alpha 3 homomeric receptors also expressed. (C) 2009 Elsevier Ireland Ltd. All rights reserved.
Formatted abstract
The amygdalar complex is a limbic structure that plays a key role in emotional processing and fear conditioning. Although inhibitory transmission in the amygdala is predominately GABA-ergic, neurons of the amygdala are also known to express glycine receptors. The subtype and function of these glycine receptors within the synaptic circuits of the amygdala are unknown. In this study, we have investigated the relative expression of the four major glycine receptor subunits (α1-3 and β) in the rat basolateral (BLA) and central amygdala (CeA), using real-time PCR and protein biochemistry. We demonstrate that α1, α2, α3, and β subunits are all expressed in the BLA and CeA with α2 being the predominant α-subunit in both nuclei. Electrophysiological recordings from BLA and CeA neurons in acute brain slices indicated that differences in relative expression of these subunits were correlated with the pharmacological properties of native glycine receptors expressed on these neurons. We conclude that glycine receptors assembled in BLA neurons are largely α1β-containing heteromultimers whereas receptors assembled in neurons of the central amygdala are primarily α2β-, α3β- or α1β-containing heteromultimers, with a minor component of α2 or α3 homomeric receptors also expressed.
© 2009 Elsevier Ireland Ltd. All rights reserved.
Keyword Amygdala
Pharmacology
Glycine receptors
Q-Index Code C1
Q-Index Status Confirmed Code
Institutional Status UQ

Document type: Journal Article
Sub-type: Article (original research)
Collections: 2010 Higher Education Research Data Collection
Queensland Brain Institute Publications
 
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Created: Fri, 15 Jan 2010, 21:15:25 EST by Debra McMurtrie on behalf of Queensland Brain Institute