This research proposal stems from two lines of evidence: (1) chronic ethanol consumption inhibits lesion-induced axon sprouting in the adult rat and (2) maternal alcohol intake during pregnancy is detrimental to brain development and function in the offspring. Sprouting and synaptic modulation are thought to play an important role in normal CNS function therefore, the overall goal of this research is to determine the consequences of alcohol exposure in utero on neuronal plasticity. This phenomenon will be examined by studying lesion-induced sprouting in the female offspring of the alcoholic rat. The habenula will be used as a deafferentation model to study neuroplasticity, since work from this laboratory has demonstrated lesion-induced noradrenergic (NA) sprouting in this brain region. A combination of biochemical and histofluorescent techniques will be used to specifically characterize NA axon sprouting. Blood alcohol levels will be measured in a separate group of pregnants. The information derived from this work will provide important information related to the functional consequences of prenatal ethanol exposure. Furthermore, it will be of interest to both fundamental neurobiologists and clinicians.
