My research is focused in elucidating how different types of external insults (such as early alcohol exposure) disrupt activity-dependent plasticity and how we can restore it.
Lab Techniques and Equipment:To devise new ways to improve plasticity in models of neuro-developmental disorders my lab uses in vivo viral-mediated gene transfer and pharmacological manipulations. The effects of these types of interventions are measured at different levels: a) Molecular- Imunohistochemistry and Imunoblotting; b) Cellular: Single-Unit electrophysiology, Staining with Neuronal tracers c) Systemic: Optical imaging of intrinsic signals; Visual evoked potentials d) Behavioral: Morris water maze, Social play behavior analysis.
Grants & Contracts:
Supported by National Institutes of Health/NIAAA, R01AA013023
Medina, A.E., Krahe, T.E., Coppola, D.M. & Ramoa, A.S. (2003) Neonatal Alcohol Exposure Induces Long-Lasting Impairment of Visual Cortical Plasticity in Ferrets. J Neurosci 23 (31): 10002-12.
Medina, A.E., Krahe, T.E. &. Ramoa, A.S. (2006) Restoration of Neuronal Plasticity by a phosphodiesterase Type 1 Inhibitor in a model of Fetal Alcohol Exposure. J. Neurosci., 26(3):1057-1060.
Krahe, T.E.; Wang, W. & Medina, A.E. (2009) Phosphodiesterase Inhibition increases CREB phosphorylation and restores Orientation Selectivity in a Model of Fetal Alcohol Spectrum Disorders. PLoS ONE 4:e6643.
Medina, A.E. (2010) Overexpression of serum response factor restores ocular dominance plasticity in a model of fetal alcohol spectrum disorders. J. Neurosci., 30(7):2513-20
Pohl-Guimaraes F, Krahe Te, Medina A.E. (2011) Early valproic acid exposure alters functional organization in the primary visual cortex. Exp Neurol. 228(1):138-48.
Medina, A.E. (2011) Therapeutic utility of phosphodiesterase type I inhibitors in neurological conditions. Front Neurosci. 18;5:21.
Medina, A.E. (2011) Fetal Alcohol Spectrum Disorders and Abnormal Neuronal Plasticity. Neuroscientist. 17(3):274-87.
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