Baclofen Does Not Counteract the Acute Effects of Ethanol on Flash-Evoked Potentials in Long-Evans Rats

Abstract

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 (VC) and superior colliculus (SC) of chronically implanted male Long-Evans rats. In the VC, 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.

Keywords:

• baclofen
• ethanol
• flash-evoked potentials
• rats
• superior colliculus
• visual cortex