This study was supported by the National Institute on Alcoholism and Alcohol Abuse (Grant AA06548 to D.D.S. and L.L.P.) and the National Institute for General Medical Science (Grant GM08139 to D.D.S., L.L.C., and L.M.D.).
Prenatal Ethanol Exposure Diminishes Activity-Dependent Potentiation of Amino Acid Neurotransmitter Release in Adult Rat Offspring
Article first published online: 30 MAY 2006
Alcoholism: Clinical and Experimental Research
Volume 22, Issue 8, pages 1771–1777, November 1998
How to Cite
Savage, D. D., Cruz, L. L., Duran, L. M. and Paxton, L. L. (1998), Prenatal Ethanol Exposure Diminishes Activity-Dependent Potentiation of Amino Acid Neurotransmitter Release in Adult Rat Offspring. Alcoholism: Clinical and Experimental Research, 22: 1771–1777. doi: 10.1111/j.1530-0277.1998.tb03978.x
- Issue published online: 30 MAY 2006
- Article first published online: 30 MAY 2006
- Received for publication January 23, 1998; accepted August 6, 1998
- Key Words:;
- Neurotransmitter Release;
- Long-Term Potentiation;
- Hippocampal Formation;
- Fetal Alcohol Syndrome
Prenatal ethanol exposure has been associated with long-lasting intellectual impairments in children. Previous studies suggest that these deficits are, in part, linked to neurochemical abnormalities that reduce the ability to sustain long-term potentiation (LTP) in hip-pocampal formation of adult offspring. One presynaptic component of LTP that manifests during the first half-hour alter tetanic stimulation is an enhancement of amino acid neurotransmitter release. Given that the onset of enhanced neurotransmitter release correlates temporally with the decay of hippocampal LTP in prenatal ethanol-exposed offspring, we tested the hypothesis that prenatal ethanol exposure reduces tetanus stimulus-induced potentiation of electrically evoked amino acid release in hippocampal slices. Rat dams consumed 1 of 3 diets throughout gestation: (1) a BioServ liquid diet containing 5% (v/v) ethanol (26% ethanol-derived calories) that produces a maternal peak blood ethanol concentration of 83 mg/dl; (2) pair-fed an isocalorically equivalent amount of 0% ethanol liquid diet; or (3) Purina rat chow ad libitum. Hippocampal slices were prepared from adult offspring from each experimental diet group. Neither the amount of hippocampal slice tissue protein nor the incorporation of [3H]-d-aspartate (D-ASP) was affected by prenatal ethanol exposure. Furthermore, spontaneous efflux and electrically evoked D-ASP release were similar among the three diet groups. However, tetanus stimulus-induced potentiation of evoked D-ASP release in prenatal ethanol-exposed offspring was reduced to about one-third of the potentiation of D-ASP release Observed in the control diet groups. These results suggest that prenatal ethanol exposure produces long-lasting deficits in the neurochemical mechanisms responsible for activity-dependent potentiation of amino acid transmitter release without affecting the synaptic machinery responsible for amino acid uptake, storage, and release.