MOLECULAR REGULATION OF GABAA RECEPTORS IN THE AMYGDALA

Emory University, Atlanta GA

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Abstract

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. Primary support for the subproject and the subproject's principal investigator may have been provided by other sources, including other NIH sources. The Total Cost listed for the subproject likely represents the estimated amount of Center infrastructure utilized by the subproject, not direct funding provided by the NCRR grant to the subproject or subproject staff. We have made considerable progress in the past year. We have completed all of the fear-related aspects and have obtained pilot data on the acute, chronic, and withdrawal of BZD treatment. We have examined the effects of the various levels of test drugs on motor locomotion (sedation), PTz-induced seizures (anticonvulsant effects), and the acquisition of Pavlovian contextual fear (amnesia) in separate cohorts of animals. We also determined what PTZ dose level (25-100 mg/kg) produced seizures both reliably and at levels which allow detection of experimentally-induced changes. We have been working to maximize our ability to silence the Gephyrin protein in vitro and in vivo with lentiviral vectors. We have continued to work with the knockout mouse line, and have worked to "rescue" GAD65 with lentivirus-mediated GAD65 expression. We have completed work on a lentiviral vector that convincingly decreases GAD67 expression, and have begun using this too for behavioral studies. We have recently published (Heldt et al., 2010, J Neurosci) data demonstrating behavioral effects of GABA(A)alpha1 deletions specifically from amgydala. We have also pioneered the use of primary amgydala cultures to examine GABA(A) receptor modulation and recycling (Mou et al., 2010, Neuroscience).