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Effects of Developmental Alcohol Exposure on Potentiation and Depression of Visual Cortex Responses
Author(s) -
Lantz Crystal L.,
Sipe Grayson O.,
Wong Elissa L.,
Majewska Ania K.,
Medina Alexandre E.
Publication year - 2015
Publication title -
alcoholism: clinical and experimental research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 153
eISSN - 1530-0277
pISSN - 0145-6008
DOI - 10.1111/acer.12775
Subject(s) - monocular deprivation , long term potentiation , visual cortex , neuroscience , neuroplasticity , long term depression , psychology , alcohol , saline , electrophysiology , ocular dominance , medicine , endocrinology , biology , nmda receptor , biochemistry , receptor , ampa receptor
Background Neuronal plasticity deficits are thought to underlie abnormal neurodevelopment in fetal alcohol spectrum disorders and in animal models of this condition. Previously, we found that alcohol exposure during a period that is similar to the last months of gestation in humans disrupts ocular dominance plasticity ( ODP ), as measured in superficial cortical layers. We hypothesize that exposure to alcohol can differentially affect the potentiation and depression of responses that are necessary for activity‐dependent sprouting and pruning of neuronal networks. ODP is an established paradigm that allows the assessment of activity‐dependent depression and potentiation of responses in vivo. Methods Mouse pups were exposed to 3.6 to 5 g/kg of ethanol in saline daily or every other day between postnatal days 4 and 9. Visual cortex plasticity was then assessed during the critical period for ODP using 2 techniques that separately record in layers 4 (visually evoked potentials [VEPs]) and 2/3 (optical imaging of intrinsic signals [OI]). Results We discovered a layer‐specific effect of early alcohol exposure. Recording of VEP s from layer 4 showed that while the potentiation component of ODP was disrupted in animals treated with alcohol when compared with saline controls, the depression component of ODP (Dc‐ ODP ) was unaltered. In contrast, OI from layers 2/3 showed that Dc‐ ODP was markedly disrupted in alcohol‐treated animals when compared with controls. Conclusions Combined with our previous work, these findings strongly suggest that developmental alcohol exposure has a distinct and layer‐specific effect on the potentiation and depression of cortical responses after monocular deprivation.