The objective of this investigation is to examine the effects of maternal alcohol treatment on perinatal differentiation of the sexually dimorphic nucleus of the preoptic area (SDN-POA). Maternal alcohol consumption during pregnancy has been shown to be detrimental to development of the fetal central nervous system. Alcohol consumption also results in depression of the gonadal steroids in male rats. Since masculine differentiation of the SDN-POA is dependent upon the presence of fetal androgens during a critical period of brain development, maternal alcohol consumption may result in the alteration of androgen dependent neuronal development producing permanent structural alteration of the SDN-POA neurons in the male offspring. The ability for maternal alcoholization to induce this defect will be examined by allowing pregnant female rats to consume an alcohol diet during gestation and then assess the structural and biochemical changes induced in the SDN-POA in male offspring. Possible mechanisms by which this developmental effect occurs will be investigated by examining brain and serum androgen levels in neonates from alcohol-treated mothers, neuronal testosterone binding in the SDN-POA region and the ability of the SDN-POA to aromatize testosterone. The reduction of androgen secretion by the perinatal tests, the loss of neuronal androgen binding or the reduction of the ability of the neonatal brain to convert testoterone to estrogen may be an indication of the mechanism by which demasculinization of the neonatal brain occurs. The alteration of fetal neuronal sexual differentiation by maternal alcohol consumption could result in abnormalities in the adult of the neuroendocrine control of reproductive events, reduced fertility, behavioral changes or yet undefined consequences.

Agency
National Institute of Health (NIH)
Institute
National Institute on Alcohol Abuse and Alcoholism (NIAAA)
Type
Research Project (R01)
Project #
5R01AA005893-03
Application #
3109165
Study Section
Alcohol Biomedical Research Review Committee (ALCB)
Project Start
1983-09-29
Project End
1986-08-31
Budget Start
1985-09-01
Budget End
1986-08-31
Support Year
3
Fiscal Year
1985
Total Cost
Indirect Cost
Name
University of Missouri-Columbia
Department
Type
Schools of Medicine
DUNS #
112205955
City
Columbia
State
MO
Country
United States
Zip Code
65211
Scott, H C; Zoeller, R T; Rudeen, P K (1995) Acute prenatal ethanol exposure and luteinizing hormone-releasing hormone messenger RNA expression in the fetal mouse brain. Alcohol Clin Exp Res 19:153-9
Rudeen, P K; Weinberg, J (1993) Prenatal ethanol exposure: changes in regional brain catecholamine content following stress. J Neurochem 61:1907-15
Scott, H C; Paull, W K; Rudeen, P K (1992) Effects of in utero ethanol exposure on the development of LHRH neurons in the mouse. Brain Res Dev Brain Res 66:119-25
Zoeller, R T; Rudeen, P K (1992) Ethanol blocks the cold-induced increase in thyrotropin-releasing hormone mRNA in paraventricular nuclei but not the cold-induced increase in thyrotropin. Brain Res Mol Brain Res 13:321-30
Creighton-Taylor, J A; Rudeen, P K (1991) Fetal alcohol exposure and effects of LHRH and PMA on LH beta-mRNA expression in the female rat. Alcohol Clin Exp Res 15:1031-5
Creighton-Taylor, J A; Rudeen, P K (1991) Prenatal ethanol exposure and opiatergic influence on puberty in the female rat. Alcohol 8:187-91
Kelce, W R; Ganjam, V K; Rudeen, P K (1990) Inhibition of testicular steroidogenesis in the neonatal rat following acute ethanol exposure. Alcohol 7:75-80
Rudeen, P K; Creighton, J; Bylund, D B et al. (1990) Ontogeny of light-induced decrease of N-acetyltransferase activity in explanted chick pineal glands. J Pineal Res 8:153-8
Kelce, W R; Ganjam, V K; Rudeen, P K (1990) Effects of fetal alcohol exposure on brain 5 alpha-reductase/aromatase activity. J Steroid Biochem 35:103-6
Rudeen, P K; Creighton, J A; Bylund, D B et al. (1990) Effects of light and an alpha-2-adrenergic agonist on serotonin N-acetyltransferase activity in chick pineal gland. J Neural Transm Gen Sect 82:119-29

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