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Abstract
Alcohol consumption during pregnancy can result in varying amounts of severity of fetal alcohol syndrome (FAS). Studies have demonstrated the relative vulnerability of the brain to the effects of alcohol exposure differ within critical times during development. There have been few studies specifically examining the effect of prenatal ethanol exposure (PE) on the hypothalamo-neurohypophyseal system.
Previous work shows that rats exposed to ethanol during embryonic days (E) 7–22 had a 20% increase in urine output, water intake and an increased osmotic threshold for AVP in PE rats than no-prenatal ethanol exposure (NPE) rats. The present studies further characterize the effects of PE and attempts to delineate human-trimester equivalent in the rat to examine a temporal effect on AVP systems in the young adult rat.
Sprague Dawley dams were fed a liquid diet with 35% of the calories from ethanol or a control. The four dietary treatments were as follows: ethanol exposure on E 1–11, E 12–22, E 1–22 and control. On the day of experiment, a series of three 10% blood volume hemorrhage samples were taken at 10-minute intervals.
Overall, PE rats drank 21.8% more than NPE, and these females drank more than their male counterparts. PE 12–22 and PE 1–22 had an augmented water intake than NPE and PE 1–11. In response to 10% hemorrhage, all groups had a significant increase of plasma AVP except for the PE 12–22 rats. A similar, but augmented trend of AVP release was seen after 20% hemorrhage. Pituitary AVP content was 14.5% lower in PE rats compared to NPE, and the PE 12–22 rats had the lowest AVP storage levels. Hypothalamic AVP mRNA was 27.8% and 35.1% lower in PE 12–22 and PE 1–22 rats compared to NPE rats respectively, and were also found to be significantly lower than PE 1–11 rats, suggesting a temporal effect.
PE has deleterious temporal effects on pituitary AVP storage, hypothalamic AVP mRNA and response to hemorrhage. PE rats displayed a blunted AVP release response to hypotensive hemorrhage, which coincided with the change in BP and HR. Furthermore, the present study shows that the defects to the vasopressinergic system due to gestational exposure to ethanol are most likely to occur during E 12–22, when the SON and PVN are being developed.
