Abstract Dr. Pierce
Developmental Ethanol Exposure and Oxidative Stress
The present study was designed to evaluate the mechanism by which a single ethanol dose delivered intragastrically on postnatal day 4 (PN 4) to rat pups triggers apoptosis of Purkinje cell neurons in the cerebellum. The hypothesis being tested is that ethanol exposure results in the death of the Purkinje neurons by inducing intracellular oxidative stress and interrupting intracellular signaling resulting in neurotrophic factor withdrawal. Data will be collected at various time points subsequent to single ethanol dose to determine the timing of events which shift intracellular signaling away from survival and towards cell death by apoptosis. Immunohistochemical techniques will be utilized to identify Purkinje neurons experiencing oxidative stress and/or alterations in intracellular signaling subsequent to ethanol exposure. Data will also be collected to test the hypothesis that antioxidant therapy can inhibit the loss of Purkinje cells, which occurs with the PN 4 ethanol exposure. The magnitude of Purkinje cell loss following ethanol exposure with or without concurrent antioxidant (N-acetylcysteine) treatment will be measured using reverse-transcriptase polymerase chain reaction (RT-PCR) techniques.
Updated 10/31/2005
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