GABAergic drugs can positively or negatively influence recovery of neurobeh
avioral function following brain injury. Direct potentiation of GABA-mediat
ed inhibition at the post-synaptic receptor (i.e., via GABA, muscimol, diaz
epam, phenobarbital) after brain damage has been associated with impaired f
unctional 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-t
ransaminase, was administered chronically after unilateral anteromedial cor
tex 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 ant
i-convulsant doses tested. Measurable secondary drug effects like sedation
and hypothermia diminished over time and were reversible upon drug disconti
nuation. These results suggest that the degree to which a GABAergic agent i
mpacts the recovery process after brain injury is dependent on the drug's m
echanism of action.