No abstract

Prenatal ethanol exposure reduces the density of the N-methyl-D-aspartate (NMDA) receptor agonist binding sites and decreases the capacity to elicit long-term potentiation (LTP) in hippocampal formation of 45-day-old rat offspring. We hypothesized that prenatal ethanol exposure would reduce metabotropic-glutamate receptor (mGluR)-activated phosphoinositide hydrolysis also. Sprague-Dawley rat dams were fed a liquid diet containing either 3.35% (v/v) ethanol or 5.0% ethanol throughout gestation. Control groups were pair-fed either isocalorically matched 0% ethanol liquid diets or lab chow ad libitum. (1S,3R)-1-aminocyclopentane-1,3-dicarboxylic acid (trans-ACPD) stimulated inositol-1-phosphate (IP1) accumulation via activation of the mGluR in offspring whose mothers consumed the 3.35% ethanol liquid diet was not different compared with the control groups. Furthermore, trans-ACPD stimulated IP1 accumulation in 10- to 13-day-old offspring of the 5.0% ethanol diet group was not different compared with the control groups. However, trans-ACPD stimulated IP1 accumulation was reduced significantly in 56- to 82-day-old offspring of dams fed the 5.0% ethanol liquid diet compared with the control groups. In contrast, bethanechol stimulated IP1 accumulation, mediated via activation of muscarinic cholinergic receptors, was not affected by maternal consumption of either ethanol liquid diet. These results suggest both dose- and age-dependent effects of prenatal ethanol exposure on hippocampal responsiveness to trans-ACPD-activated phosphoinositide hydrolysis. Furthermore, the ability of the 3.35% ethanol diet to alter hippocampal NMDA receptors without altering the mGluR response suggests a differential sensitivity to the effects of ethanol exposure in utero among hippocampal glutamate receptor subtypes.(ABSTRACT TRUNCATED AT 250 WORDS)

Free calcium ion concentration (mmol/l) and pH were determined in whole blood using a semiautomatic electrode system (ICA-1 Radiometer, Copenhagen, Denmark) in 37 normal women, 90 pregnant women (30 from each trimester of gestation), 28 mothers at delivery and their respective newborns. The blood samples from normal controls, pregnant women, umbilical cord and 40-50-hour-old infants were collected anaerobically in vacuum tubes. Duplicate samples drawn from newborns shortly after birth by heel puncture were collected in special heparinized capillary tubes. We observed that Ca2+ concentrations in the second (1.20 +/- 0.04) and third (1.20 +/- 0.05) trimesters of pregnancy, and at delivery (1.18 +/- 0.05), were lower than in the control group (1.23 +/- 0.04). The [Ca2+] in samples from the umbilical vein (1.44 +/- 0.11) and artery (1.45 +/- 0.08) and from newborns 2-5 min after birth (1.34 +/- 0.12) was greater than in control samples. The [Ca2+] in newborns 40-50 hours after birth was lower (1.16 +/- 0.14) than in the control group.