Modulation of responses to visual stimulus onset and offset by chronic alcohol consumption and withdrawal in the rat visual cortex and lateral geniculate nucleus

In the visual system, chronic alcohol consumption and subsequent abstinence strongly modulate processing of sensory information, which could interfere with the actions in our daily lives. Although previous studies showed histological and electrophysiological changes in the retina and visual cortex during chronic alcohol consumption and abstinence, there is still a lack of information related to the effect of alcohol on: 1) different stages of visual information processing; and 2) responses of stimulus onset (ON) and offset (OFF). In order to answer these questions, we recorded visual evoked potentials (VEPs), elicited by onset and offset of a 500-ms stimulus, following long-term alcohol consumption (8 weeks) and abstinence (3 weeks) in freely moving Wistar rats. Latency and amplitude of five components in the visual cortex (N1(VC), P2(VC), N2(VC), P3(VC), N3(VC)) and three components in the lateral geniculate nucleus (P1(LGN), N1(LGN), P2(LGN)) were analyzed. The results showed that long-term chronic alcohol consumption and abstinence have a strong long-term and, in some cases, irreversible impact on visual information processing. Both of these conditions modulate only the last stage of stimulus onset processing at the level of the visual cortex, but not at the level of the lateral geniculate body. Response to the stimulus offset is more susceptible to the effect of alcohol consumption and/or abstinence and is modulated at both the visual cortex and lateral geniculate nucleus levels. This modulation at different stages of the information processing chain can result in inaccurate processing of visual stimuli parameters and can lead to changes in perception of stimulus duration and intensity. (C) 2019 Elsevier Inc. All rights reserved.