Baclofen does not counteract the acute effects of ethanol on flash-evoked potentials in Long-Evans rats.

This experiment examined the separate and combined effects of baclofen (5.0 mg/kg, i.p.), a GABA B receptor agonist, and ethanol (2.0 g/kg, i.p.) on flash-evoked potentials (FEPs) recorded from both the visual cortex and superior colliculus (SC) of chronically implanted male Long-Evans rats. In the visual cortex, ethanol significantly decreased the amplitude of positive component P87, but increased P37 and P47. Other component amplitudes were not significantly altered. In contrast, baclofen reduced the amplitude of negative component N31 to such an extent that it became positive. Although P47 was also reduced by baclofen, the amplitude of most other components was increased. Only P24 and P87 were unchanged by baclofen. The combination of baclofen and ethanol resulted in amplitudes very similar to ethanol alone for secondary components P47, N62, and P87, but very similar to baclofen alone for primary component N31 and late components N147 and P230. In the SC, component amplitudes were generally decreased by ethanol, baclofen, and the combination treatment. Latencies of most components in both structures were increased by the drug treatments. Each drug treatment produced significant hypothermia. Locomotor behavior was also altered. These results demonstrate: (1) pharmacological differences between the primary and late components versus the secondary components of the cortical FEP, (2) that baclofen does not counteract significant effects of ethanol on cortical or collicular component amplitudes, and (3) that baclofen enhances N147-P230 amplitude, suggesting reduced cortical arousal.