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The Journal of Neuroscience, January 12, 2005, 25(2):502-506; doi:10.1523/JNEUROSCI.3301-04.2005

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BRIEF COMMUNICATION
Regulation of Gephyrin and GABA_A Receptor Binding within the Amygdala after Fear Acquisition and Extinction

Jasmeer P. Chhatwal, Karyn M. Myers, Kerry J. Ressler, and Michael Davis

Department of Psychiatry and Behavioral Sciences and Center for Behavioral Neuroscience, Emory University School of Medicine, Atlanta, Georgia 30322

Both the acquisition and extinction of conditioned fear appear to require the basolateral amygdala (BLA). Because these two forms of learning have opposing effects on the expression of conditioned fear, we hypothesized that they may modulate GABAergic tone differentially within the BLA. Previously, we reported that gene expression for the GABA_A receptor clustering protein gephyrin was significantly downregulated in the BLA after fear acquisition (Ressler et al., 2002). Here we demonstrate an analogous decrease in BLA gephyrin protein levels, together with a decrease in the surface expression of GABA_A receptors in the BLA after fear acquisition, as evidenced by decreased binding of H3-flunitrazepam. In marked contrast, gephyrin mRNA and protein levels in the BLA significantly increased after extinction training, as did H3-flunitrazepam binding. These results implicate the protein gephyrin in both fear acquisition and extinction and suggest that the modulation of gephyrin and GABA_A receptor expression in the BLA may play a role in the experience-dependent plasticity underlying both of these types of learning. Furthermore, these results demonstrate that physiologically relevant, dynamic alterations of GABAergic synapses occur during the consolidation phase of BLA-dependent learning and may interact with previously described alterations in glutamatergic transmission to initiate and stabilize memory formation in vivo.

Key words: amygdala; autoradiography; extinction; fear; GABA (-aminobutyric acid); learning

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Received April 26, 2004; revised November 18, 2004; accepted November 22, 2004.

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