Affiliations: Behavioral Neuroscience Program, Department of Psychology, Campus Box 345, The University of Colorado, Boulder, CO 80309, USA
Abstract: GABAergic drugs can positively or negatively influence recovery of
neurobehavioral function following brain injury. Direct potentiation of
GABA-mediated inhibition at the post-synaptic receptor (i.e., via GABA,
muscimol, diazepam, phenobarbital) after brain damage has been associated with
impaired functional recovery. What remains unclear, however, is whether the
mechanism of action by which GABA is augmented contributes to a drug's impact
on the recovery process. Vigabatrin, a novel anti-convulsant that inhibits
GABA-transaminase, was administered chronically after unilateral anteromedial
cortex lesions and recovery from somatosensory deficits assessed. In contrast to the direct GABA receptor agonists, vigabatrin did not adversely impact (i.e., was neutral) recovery from neurobehavioral deficits at any of the
anti-convulsant doses tested. Measurable secondary drug effects like sedation
and hypothermia diminished over time and were reversible upon drug
discontinuation. These results suggest that the degree to which a GABAergic
agent impacts the recovery process after brain injury is dependent on the drug's
mechanism of action.
Keywords: GABA, anteromedial cortex lesion, somatosensory asymmetry, rat, behavior, pharmacotherapy
