A Specific class of interneuron mediates inhibitory plasticity in the lateral amygdala

Polepalli, Jai S., Sullivan, Robert K. P., Yanagawa, Yuchio and Sah, Pankaj (2010) A Specific class of interneuron mediates inhibitory plasticity in the lateral amygdala. Journal of Neuroscience, 30 44: 14619-14629. doi:10.1523/JNEUROSCI.3252-10.2010

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Author Polepalli, Jai S.
Sullivan, Robert K. P.
Yanagawa, Yuchio
Sah, Pankaj
Title A Specific class of interneuron mediates inhibitory plasticity in the lateral amygdala
Journal name Journal of Neuroscience   Check publisher's open access policy
ISSN 0270-6474
Publication date 2010-11-01
Sub-type Article (original research)
DOI 10.1523/JNEUROSCI.3252-10.2010
Open Access Status File (Publisher version)
Volume 30
Issue 44
Start page 14619
End page 14629
Total pages 11
Place of publication New York, N.Y., United States
Publisher Society for Neuroscience
Language eng
Formatted abstract
The lateral amygdala (LA) plays a key role in emotional learning and is the main site for sensory input into the amygdala. Within the LA, pyramidal neurons comprise the major cell population with plasticity of inputs to these neurons thought to underlie fear learning. Pyramidal neuron activity is tightly controlled by local interneurons, and GABAergic modulation strongly influences amygdala-dependent learning. Synaptic inputs to some interneurons in the LA can also undergo synaptic plasticity, but the identity of these cells and the mechanisms that underlie this plasticity are not known. Here we show that long-term potentiation (LTP) in LA interneurons is restricted to a specific type of interneuron that is defined by the lack of expression of synaptic NR2B subunits. We find that LTP is only present at cortical inputs to these cells and is initiated by calcium influx via calcium-permeable AMPA receptors. LTP is maintained by trafficking of GluR2-lacking AMPA receptors that require an interaction with SAP97 and the actin cytoskeleton. Our results define a novel population of interneurons in the LA that control principal neuron excitability by feed-forward inhibition of cortical origin. This selective enhanced inhibition may contribute to reducing the activity of principal neurons engaged during extinction of conditioned fear. Copyright © 2010 the authors.
Keyword Long-term Potentiation
Rat Basolateral Amygdala
Parvalbumin-positive Interneurons
Glutamate-receptor Channels
Synaptic Nmda Receptors
Ampa Receptors
Hippocampal Interneurons
Conditioned fear
Q-Index Code C1
Q-Index Status Confirmed Code
Institutional Status UQ
Additional Notes Received June 23, 2010; revised Aug. 3, 2010; accepted Aug. 31, 2010.

Document type: Journal Article
Sub-type: Article (original research)
Collections: Official 2011 Collection
Queensland Brain Institute Publications
Centre for Microscopy and Microanalysis Publications
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Citation counts: TR Web of Science Citation Count  Cited 29 times in Thomson Reuters Web of Science Article | Citations
Scopus Citation Count Cited 28 times in Scopus Article | Citations
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Created: Sun, 21 Nov 2010, 10:03:04 EST