Effects of ethanol on flash-evoked potentials of rats: lack of antagonism by naltrexone.

The present study examined the effects of ethanol and naltrexone hydrochloride (a nonselective opiate receptor antagonist) on flash-evoked potentials recorded from both the visual cortex (VC) and the superior colliculus (SC) of chronically implanted hooded rats. There were four treatment conditions administered on separate days: Either saline or naltrexone (10 mg/kg; volume of 1.0 ml/kg) was given 10 min before either saline or ethanol (2.0 g/kg; 20% ethanol solution in a volume of 1.26 ml/100 g). Evoked potentials were recorded 15 min after the intraperitoneal injections were completed. Animals were tested at 23.1 degrees C room temperature. In the VC, ethanol significantly decreased the amplitude of components N1, P3, and N3, whereas it increased the amplitude of P2. Components P1 and N2 were unaffected by ethanol treatment. The SC components P3 and N4 were reduced in amplitude by ethanol, but component P1 was not altered. Latencies of all components in both structures were increased by ethanol. Naltrexone alone did not significantly affect the potentials, nor did naltrexone pretreatment significantly alter the effects of ethanol on the potentials. Naltrexone produced a modest hypothermia of about 0.25 degrees C, whereas ethanol resulted in hypothermia of about 1.0 degrees C. Ethanol, either alone or in combination with naltrexone, significantly reduced body movement during the evoked-potential recording sessions. The results indicate that endogenous opioid systems do not play a major role in the acute effects of ethanol on flash-evoked potentials recorded from primary areas of the visual system.