Prenatal Alcohol Exposure Damages Brain Signal Transduction Systems
Abstract
This report details our progress during the first year of a three-year proposal. The proposal's overall goal is to uncover biochemical mechanisms that underlie learning and memory deficits resulting from fetal alcohol exposure (FAE). We have found that adult rats that were exposed to alcohol prenatally display a decrement in learned fear. One and twenty-four hours following fear conditioning this learning deficit is associated with altered brain signal transduction mechanisms that are dependent on an enzyme termed phosphatidylinositol-specific phospholipase C-Beta 1a (PLC-Beta 1a). Tissue has been collected, and will be analyzed during the second year of the proposal, at additional times following fear conditioning. We have initiated studies aimed at elucidating the biochemical basis of the effects of FAE on PLC-beta 1a enzyme activity. Our preliminary results indicate that brain PLC-beta 1a forms a tight complex with protein kinase C, which has been implicated as playing an essential role in learning and memory. In the coming year, we will assess the effects of prenatal alcohol exposure on this association. The next phase of these studies are expected to yield important information about the neurochemical mechanisms that underlie fear and stress, and, consequently, may provide insight into the neurochemical basis of posttraumatic stress syndrome.
Document Details
- Document Type
- Technical Report
- Publication Date
- Sep 01, 2001
- Accession Number
- ADA398260
Entities
People
- Kevin K. Caldwell
Organizations
- University of New Mexico