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The Journal of Neuroscience, November 5, 2003, 23(31):10002-10012

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Development/Plasticity/Repair
Neonatal Alcohol Exposure Induces Long-Lasting Impairment of Visual Cortical Plasticity in Ferrets

Alexandre E. Medina,¹ Thomas E. Krahe,¹ David M. Coppola,^2,3 and Ary S. Ramoa¹

¹Department of Anatomy and Neurobiology, Virginia Commonwealth University School of Medicine, Richmond, Virginia 23298-0709, ²Department of Cellular Biology and Anatomy, Louisiana State University Health Sciences Center, Shreveport, Louisiana 71130-3932, and ³Department of Biology, Centenary College, Shreveport, Louisiana 71104

Fetal alcohol syndrome is a major cause of learning and sensory deficits. These disabilities may result from disruption of neocortex development and plasticity. Alcohol exposure during the third trimester equivalent of human gestation may have especially severe and long-lasting consequences on learning and sensory processing, because this is when the functional properties and connectivity of neocortical neurons start to develop. To address this issue, we used the monocular deprivation model of neural plasticity, which shares many common mechanisms with learning. Ferrets were exposed to ethanol (3.5 mg/kg, i.p.) on alternate days for 3 weeks starting on postnatal day (P) 10. Animals were then monocularly deprived at the peak of ocular dominance plasticity after a prolonged alcohol-free period (15-20 d). Quantitative single-unit electrophysiology revealed that alcohol exposure disrupted ocular dominance plasticity while preserving robust visual responses. Moreover, optical imaging of intrinsic signals revealed that the reduction in visual cortex area driven by the deprived eye was much less pronounced in ethanol-treated than in control animals. Alcohol exposure starting at a later age (P20) did not disrupt ocular dominance plasticity, indicating that timing of exposure is crucial for the effects on visual plasticity. In conclusion, alcohol exposure during a brief period of development impairs ocular dominance plasticity at a later age. This model provides a novel approach to investigate the consequences of fetal alcohol exposure and should contribute to elucidate how alcohol disrupts neural plasticity.

Key words: alcohol; ocular dominance plasticity; visual development; ferret; monocular deprivation; optical imaging; neocortex development; fetal alcohol syndrome

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Received June 3, 2003; revised September 8, 2003; accepted September 9, 2003.

This article has been cited by other articles:

				A. E. Medina, T. E. Krahe, and A. S. Ramoa Restoration of Neuronal Plasticity by a Phosphodiesterase Type 1 Inhibitor in a Model of Fetal Alcohol Exposure J. Neurosci., January 18, 2006; 26(3): 1057 - 1060. [Abstract] [Full Text] [PDF]

				A. E. Medina, T. E. Krahe, and A. S. Ramoa Early Alcohol Exposure Induces Persistent Alteration of Cortical Columnar Organization and Reduced Orientation Selectivity in the Visual Cortex J Neurophysiol, March 1, 2005; 93(3): 1317 - 1325. [Abstract] [Full Text] [PDF]

				D. S. Liao, T. E. Krahe, G. T. Prusky, A. E. Medina, and A. S. Ramoa Recovery of Cortical Binocularity and Orientation Selectivity After the Critical Period for Ocular Dominance Plasticity J Neurophysiol, October 1, 2004; 92(4): 2113 - 2121. [Abstract] [Full Text] [PDF]

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