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.

Agency
National Institute of Health (NIH)
Institute
National Institute on Alcohol Abuse and Alcoholism (NIAAA)
Type
Unknown (R23)
Project #
5R23AA006158-03
Application #
3445139
Study Section
Alcohol Biomedical Research Review Committee (ALCB)
Project Start
1984-09-01
Project End
1987-08-31
Budget Start
1986-09-01
Budget End
1987-08-31
Support Year
3
Fiscal Year
1986
Total Cost
Indirect Cost
Name
University of Texas Health Science Center Houston
Department
Type
Schools of Medicine
DUNS #
City
Houston
State
TX
Country
United States
Zip Code
77225
Gottesfeld, Z; Abel, E L (1991) Maternal and paternal alcohol use: effects on the immune system of the offspring. Life Sci 48:1-8
Gottesfeld, Z; LeGrue, S J (1990) Lactational alcohol exposure elicits long-term immune deficits and increased noradrenergic synaptic transmission in lymphoid organs. Life Sci 47:457-65
Gottesfeld, Z; Morgan, B; Perez-Polo, J R (1990) Prenatal alcohol exposure alters the development of sympathetic synaptic components and of nerve growth factor receptor expression selectivity in lymphoid organs. J Neurosci Res 26:308-16
Gottesfeld, Z; Silverman, P B (1990) Developmental delays associated with prenatal alcohol exposure are reversed by thyroid hormone treatment. Neurosci Lett 109:42-7
Gottesfeld, Z; Garcia, C J; Lingham, R B et al. (1989) Prenatal ethanol exposure impairs lesion-induced plasticity in a dopaminergic synapse after maturity. Neuroscience 29:715-23
Swann, A C; Gottesfeld, Z (1987) Deafferentation elicits a transient decrease in Na+, K+-ATPase activity and ouabain binding in the olfactory tubercle. Brain Res 404:323-6
Gottesfeld, Z; Liehr, J G (1987) Chronic exposure to random restraint stress retards the development of estrogen-induced pituitary prolactinoma in rats. Neurosci Lett 80:44-8
Lingham, R B; Gottesfeld, Z (1986) Deafferentation elicits increased dopamine-sensitive adenylate cyclase and receptor binding in the olfactory tubercle. J Neurosci 6:2208-14
Wiggins, R C; Gottesfeld, Z (1986) Restraint stress during late pregnancy in rats elicits early hypermyelination in the offspring. Metab Brain Dis 1:197-203