Increased anxiety-like behavior and enhanced synaptic efficacy in the amygdala of GluR5 knockout mice

Long Jun Wu, Shanelle W. Ko, Hiroki Toyoda, Ming Gao Zhao, Hui Xu, Kunjumon I. Vadakkan, Ming Ren, Eva Knifed, Fanny Shum, Jessica Quan, Xue Han Zhang, Min Zhuo

Research output: Contribution to journalArticlepeer-review

61 Scopus citations


GABAergic transmission in the amygdala modulates the expression of anxiety. Understanding the interplay between GABAergic transmission and excitatory circuits in the amygdala is, therefore, critical for understanding the neurobiological basis of anxiety. Here, we used a multi-disciplinary approach to demonstrate that GluR5-containing kainate receptors regulate local inhibitory circuits, modulate the excitatory transmission from the basolateral amygdala to the central amygdala, and control behavioral anxiety. Genetic deletion of GluR5 or local injection of a GluR5 antagonist into the basolateral amygdala increases anxiety-like behavior. Activation of GluR5 selectively depolarized inhibitory neurons, thereby increasing GABA release and contributing to tonic GABA current in the basolateral amygdala. The enhanced GABAergic transmission leads to reduced excitatory inputs in the central amygdala. Our results suggest that GluR5 is a key regulator of inhibitory circuits in the amygdala and highlight the potential use of GluR5-specific drugs in the treatment of pathological anxiety.

Original languageEnglish (US)
Article numbere167
JournalPloS one
Issue number1
StatePublished - Jan 24 2007

ASJC Scopus subject areas

  • General


Dive into the research topics of 'Increased anxiety-like behavior and enhanced synaptic efficacy in the amygdala of GluR5 knockout mice'. Together they form a unique fingerprint.

Cite this