Effects of chronic prenatal ethanol exposure on cGMP content and glutamate release in the hippocampus of the neonatal guinea pig.

The glutamate-N-methyl-D-aspartate (NMDA) receptor-nitric oxide synthase (NOS)-cGMP signal transduction system plays key neurotrophic and intercellular communication roles in the hippocampus. In the guinea pig, chronic prenatal ethanol exposure (CPEE), via maternal ethanol administration, suppresses the hippocampal glutamate-NMDA receptor-NOS pathway in the near-term fetus and decreases stimulated glutamate release in the hippocampus of young postnatal offspring, with no effect on NMDA receptor number or NOS activity. At present, the effect of CPEE on cGMP, a key second messenger of the glutamate signal transduction system, in the hippocampus is not known.

In vitro ethanol exposure decreases potassium-stimulated, but not veratridine-stimulated, glutamate release in the guinea pig hippocampus.

In this study we determined the effect of in vitro ethanol exposure on stimulated glutamate release in transverse hippocampal slices (400-microm thickness) of the young postnatal guinea pig (PD 12) by using two chemical stimuli with different mechanisms of action. Ethanol (50 mM) decreased K+ (45 mM)-, but not veratridine (10 microM)-, stimulated glutamate release. The study findings demonstrate that in vitro ethanol exposure produces differential inhibition of stimulated glutamate release in the hippocampus, dependent on the stimulating agent.

Generation of a high-density rat EST map.

We have developed a high-density EST map of the rat, consisting of >11,000 ESTs. These ESTs were placed on a radiation hybrid framework map of genetic markers spanning all 20 rat autosomes, plus the X chromosome. The framework maps have a total size of approximately 12,400 cR, giving an average correspondence of 240 kb/cR.

Effects of chronic prenatal ethanol exposure on hippocampal glutamate release in the postnatal guinea pig.

This study was designed to test the hypothesis that chronic prenatal ethanol exposure decreases basal and stimulated L-glutamate release in the hippocampus of young, postnatal guinea pigs. Timed, pregnant guinea pigs were randomly assigned to one of the following three chronic treatment groups: 4 g ethanol/kg maternal body weight/day, isocaloric-sucrose and pair-feeding to the ethanol group, and water. Each oral treatment was given daily throughout gestation.

Effects of chronic prenatal ethanol exposure on locomotor activity, and hippocampal weight, neurons, and nitric oxide synthase activity of the young postnatal guinea pig.

Decreased nitric oxide synthase (NOS)-catalyzed formation of NO from L-arginine may be involved in ethanol teratogenesis involving the hippocampus. This hypothesis was tested by determining the effects of chronic prenatal ethanol exposure on locomotor activity and on hippocampal weight, number of CA1 and CA3 pyramidal cells and dentate gyrus granule cells, and NOS activity of the postnatal guinea pig. Timed, pregnant guinea pigs received one of the following chronic oral regimens throughout gestation: 4 g ethanol/kg maternal body weight/day, isocaloric-sucrose/pair-feeding, or water.