Defense Date

2000

Document Type

Thesis

Degree Name

Master of Science

Department

Psychology

First Advisor

Robert J. Hamm

Abstract

Traumatic brain injury (TBI) disrupts ionic balance and produces acute widespread depolarization. Restoration of ionic balance and neuronal function after TBI may be achieved by increasing inhibitory neurotransmission (e.g., stimulating GABA-A receptors). This study used antibodies specific for β2/3 subunits to examine changes in GABA-A receptors in the rat hippocampus 24 hours following moderate fluid percussion TBI. The β2/ 3 antibody primarily stained dendritic processes. No injury related changes were found in the CA1 but extensive morphological dendritic alterations were found in the CA3 region of the hippocampus. Analysis revealed decreased length of immunoreactive processes in CA3 apical dendrites of injured animals. These changes may represent a sublethal cytoskeletal response to excessive neuroexcitation. Administration of diazepam 15 minutes prior to injury augmented IR β2/3 processes compared to injured/vehicle and sham groups. This study illustrates that GABA-A receptors are altered following TBI and these alterations may be attenuated by increasing inhibitory neurotransmission.

Comments

Scanned, with permission from the author, from the original print version, which resides in University Archives.

Rights

© The Author

Is Part Of

VCU University Archives

Is Part Of

VCU Theses and Dissertations

Date of Submission

4-20-2017

Included in

Psychology Commons

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