Nicotine–ethanol interactions in flash-evoked potentials and behavior of Long-Evans rats

Although nicotine and ethanol are often used together, little is known about their combined effects on visual system electrophysiology. This experiment examined the separate and combined effects of nicotine and ethanol on flash-evoked potentials (FEPs) recorded from both the visual cortex (VC) and superior colliculus (SC) of chronically implanted male Long-Evans rats. There were four treatment conditions administered on separate days: either saline or ethanol (2.0 g/kg, i.p.) was given 10 min before either saline or nicotine (1.0 mg/kg, s.c.). FEPs were recorded at 5, 20, and 40 min following the second injection. In the VC, ethanol significantly decreased the amplitude of most components, but increased P46. Peaks P22 and N53 were unchanged. Nicotine enhanced most component amplitudes, but decreased N29 and P234, while P22 and N139 were unchanged. In the SC, ethanol depressed the amplitude of all components studied. In contrast, nicotine significantly depressed only P27 and N48. Latencies of most components in both structures were increased by ethanol, nicotine, and the combination treatment, although a nicotine-induced enhancement of the effects of ethanol on latencies was not typically observed. Each drug treatment also produced significant hypothermia, with the combination treatment resulting in the greatest hypothermia. Ethanol, either alone or in combination with nicotine, significantly reduced body movements during the FEP recording sessions. In subsequent open-field observations, ethanol, but not nicotine, significantly increased the number of squares crossed, while the combination treatment produced the greatest increase in movement. Nicotine significantly increased rearing behavior, but both ethanol and the combination treatment eliminated rearings. Overall, data suggesting that nicotine can counteract some of the effects of ethanol was demonstrated in varying degrees in the amplitude of VC components N39, P46, N53, N65, and P88, the latency of VC component N53, the amplitude of SC component N59, and the latency of SC components N48 and N54. In contrast, a nicotine-induced enhancement of the effects of ethanol was found for only the latency of VC components N39, P88, and P234, body temperature, and open-field ambulation.