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The Journal of Neuroscience, January 26, 2005, 25(4):977-984; doi:10.1523/JNEUROSCI.4059-04.2005

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Neurobiology of Disease
Altered Behavioral Responses to Noxious Stimuli and Fear in Glutamate Receptor 5 (GluR5)- or GluR6-Deficient Mice

Shanelle Ko, ^* Ming-Gao Zhao, ^* Hiroki Toyoda, ^* Chang-Shen Qiu, and Min Zhuo

Department of Physiology, Faculty of Medicine, and Centre for the Study of Pain, University of Toronto, Toronto, Ontario M5S 1A8, Canada

Different kainate receptor (KAR) subtypes contribute to the regulation of both excitatory and inhibitory transmission. However, no study has reported a role for KAR subtypes in behavioral responses to persistent pain and fear memory. Here we show that responses to capsaicin or inflammatory pain were significantly reduced in mice lacking glutamate receptor 5 (GluR5) but not GluR6 subunits. In classic fear-memory tests, mice lacking GluR6 but not GluR5 showed a significant reduction in fear memory when measured 3, 7, or 14 d after training. Additionally, synaptic potentiation was significantly reduced in the lateral amygdala of GluR6 but not GluR5 knock-out mice. Our findings provide evidence that distinct KAR subtypes contribute to chemical/inflammatory pain and fear memory. Selectively targeting different KAR subtypes may provide a useful strategy for treating persistent pain and fear-related mental disorders.

Key words: kainate receptor; fear memory; inflammatory pain; capsaicin; complete Freund's adjuvant; knock-out mice

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Received May 27, 2004; revised November 23, 2004; accepted December 13, 2004.

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