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. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. We made considerable progress during the reporting period. We completed all of the fear-related aspects and obtained pilot data on the acute, chronic, and withdrawal of BZD treatment. We 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 determined what PTZ dose level (25-100 mg/kg) produced seizures both reliably and at levels which allowed detection of experimentally-induced changes. We worked to maximize our ability to silence the Gephyrin protein in vitro and in vivo with lentiviral vectors. We continued to work with the knockout mouse line, and worked to "rescue" GAD65 with lentivirus-mediated GAD65 expression. We completed work on a lentiviral vector that convincingly decreases GAD67 expression, and began using this tool for behavioral studies.