Prenatal Alcohol Exposure Damages Brain Signal Transduction Systems
Abstract
This report details our progress during the second 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 made three important novel observations: First, we found that FAE increases the amount of PLC activity associated with extracellular signal-regulated kinase 2 (ERK2) in the hippocampal formation isolated from control animals. Second, we found that FAE modifies the effect of fear conditioning on the association between ERK2 and phospholipase C (PLC). Third, we identified that ERK2 associates with PLC-beta and PLC-gamma isozymes in rat hippocampal formation. Finally, we have initiated studies on the effect of ERK2-dependent phosphorylation on of PLC on PLC enzyme activity. In addition to increasing our understanding of the biochemical basis of FAE-induced learning deficits, the next phase of these studies is 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, 2002
- Accession Number
- ADA412840
Entities
People
- Kevin K. Caldwell
Organizations
- University of New Mexico