Le present article a pour but de reviser l'etat actuel des connaissances de la teratogenese neuro-comportementale de l'ethanol et de ses mecanismes hypothetiques. La revision examine la teratogenese de l'ethanol chez l'humain, incluant le syndrome d'alcoolisme foetal, et chez des animaux experimentaux. Plusieurs mecanismes hypothetiques de la teratogenese neuro-comportementale de l'ethanol sont discutes : role de l'acetaldehyde en tant que metabolite immediat de l'ethanol, hypoxie foetale, dysfonctionnement placentaire, metabolisme des prostaglandines foetales et action de l'ethanol sur les neurones du cerveau foetal, incluant l'hippocampe, l'une des principales cibies de l'ethanol. L'effet de l'ethanol sur la liberation de L-glutamate, un neurotransmetteur excitateur des acides amines, dans l'hippocampe foetal, est decrit. De plus, le role du L-glutamate dans la teratogenese de l'ethanol mettant en jeu l'hippocampe, est discute. Un nouveau mecanisme associe au developpement neuronal anormal dans l'hippocampe foetal, provoque par une exposition prenatale a l'ethanol, est presente. Enfin, des experiences visant a verifier cette hypothese sont proposees.

Ethanol neurobehavioural teratogenesis and the role of L-glutamate in the fetal hippocampus

Background : Although the mechanisms that underlie fetal alcohol-induced neuronal loss have not been determined, hypoxia/hypoxemia has been considered a leading candidate. This study was designed to test the hypothesis that neuronal loss could occur in the developing brain in the absence of fetal hypoxemia.



Methods: Three groups of pregnant sheep were used: a control group, a binge-drinking group, and a pair-fed group. The alcohol and pair-fed animals were anesthetized on day 113 of pregnancy, and the mothers and fetuses were instrumented with arterial and venous catheters. All animals were killed on day 133. Stereological cell counting techniques were used to estimate the total number of Purkinje cells in the fetal cerebellum.



Results: Peak maternal and fetal blood alcohol concentrations did not produce fetal hypoxemia. Nevertheless, there was a 25% loss of Purkinje cells of the cerebellum in the alcohol-exposed fetuses compared with that in the pair-fed controls. The loss of neurons was not accompanied by microencephaly or a concomitant decrease in either cerebellar weight or volume of the fetal cerebellum.



Conclusions: Neuronal loss can be observed after alcohol exposure during the third trimester equivalent in fetal sheep in the absence of alcohol-induced hypoxemia. Furthermore, cell loss in the absence of deficits in gross brain weight or regional brain volume indicates that the lack of gross brain volume deficits from magnetic resonance imaging techniques is not a reliable indication that the brain is unaffected by the alcohol exposure.

Alcohol‐Mediated Purkinje Cell Loss in the Absence of Hypoxemia During the Third Trimester in an Ovine Model System

Background: The mechanisms by which maternal ethanol abuse during pregnancy causes neurodevelopmental injury in the fetus are not well understood The purpose of this study was to use a chronically instrumented fetal sheep model system to determine if a binge pattern of ethanol exposure administered throughout the third trimester reduced fetal arterial partial pressure of oxygen (P a O 2 ); a positive finding would support the hypothesis that fetal hypoxemia may play a role in mediating ethanol-related birth defects Methods: Pregnant ewes received saline or 075, 125, 15, or 175 g/kg of ethanol intravenously over 1 hr beginning on day 109 of gestation (term = 145 days) for 3 consecutive days per week followed by 4 days without exposure The fetuses were surgically instrumented on day 113, and experiments were performed on days 118 or 132, the 6th and the 12th ethanol exposure, respectively Results: Ethanol infusions resulted in peak blood ethanol concentrations of 808 ± 65, 1825 ± 135, 2244 ± 139, and 2606 ± 200 mg/dl ± SEM (maternal) and 700 ± 59, 1497 ± 90, 2169 ± 140, and 2333 ± 198 mg/dl ± SEM (fetal) in response to the 075, 125, 15, and 175 g/kg doses, respectively Maternal and fetal heart rate and maternal blood pressure increased whereas fetal blood pressure decreased in a dose-dependent manner in response to ethanol infusions Maternal and fetal arterial pH decreased and arterial partial pressures of carbon dioxide increased in response to ethanol infusions Maternal P a O 2 decreased whereas fetal P a O 2 did not change in response to ethanol infusions Conclusions: A binge ethanol exposure paradigm, three consecutive days per week throughout the third trimester at ethanol doses that created blood ethanol concentrations commonly achieved by human ethanol abusers, resulted in changes in maternal and fetal heart rate, changes in blood pressure, hypercapnea, acidemia, and maternal, but not fetal, hypoxemia We conclude that in an ovine model system, ethanol doses that create blood ethanol concentrations as high as 260 mg/dl do not result in fetal hypoxemia Remaining issues to address with this model system are whether neurodevelopmental injuries that are associated with maternal ethanol abuse are mediated by a reduction in fetal cerebral blood flow, fetal hypercapnea, or acidemia

Third trimester binge ethanol exposure results in fetal hypercapnea and acidemia but not hypoxemia in pregnant sheep.

The purpose of this review is to critically examine the effects of ethanol on the embryo-fetus. There has been a tremendous amount of human epidemiological and experimental animal research on the characterization of the anomalies produced by chronic prenatal ethanol exposure and the identification of critical periods of vulnerability and critical amounts of ethanol necessary to produce fetal effects and (or) abnormal development. Few studies have examined the underlying mechanism(s) of the action of ethanol, and even fewer studies have examined the effects of single-dose ethanol exposure on the embryo-fetus. In this review, the current state of knowledge of the effects of chronic use of ethanol on the embryo-fetus is summarized. The primary focus of the review is on the embryonic-fetal effects of acute ethanol exposure, with particular emphasis on the ethanol-induced suppression of fetal breathing movements, as this effect appears to be a very sensitive index of acute exposure of the near-term fetus to ethanol. Factors to be considered in the selection of experimental animals to investigate the mechanism of action of ethanol and to study the acute effects of ethanol are discussed. Postulated mechanisms of action of ethanol on the embryo-fetus are evaluated with a focus on the role of prostaglandins. Finally, future directions in this field of research are proposed.

Effects of ethanol exposure on the embryo-fetus: experimental considerations, mechanisms, and the role of prostaglandins.

Ocular malformations and visual deficits are pathognomic of fetal alcohol syndrome (FAS). However, there are no reports on retinal visual function. To determine if prenatal (human second-trimester equivalent) or prenatal plus 10 days of postnatal (human third-trimester equivalent) ethanol exposure produced scotopic and/or photopic deficits in adult hooded rats, electroretinography (ERG) was used to examine rod and cone, increment threshold, dark adaptation, and paired-flash amplitude recovery functions. The rhodopsin content per eye also was determined. Five main results were found. First, voltage-log intensity and latency-log intensity functions, generated from single-flash ERGs in fully dark-adapted rats, showed increases in absolute threshold and latency and decreases in response amplitude. Second, cone ERGs had latency increases. Third, there were decreases in the scotopic and photopic critical flicker-fusion frequencies, increment threshold functions, and absolute and relative refractory periods. Fourth, rod sensitivity, range, and rate of dark adaptation were decreased. Fifth, rhodopsin content per eye was decreased. These data showed that prenatal ethanol exposure produces long-term deficits in retinal sensitivity, amplitude, light and dark adaptation, temporal processing, and excitability. Larger deficits occurred in the scotopic than photopic system and were produced with an additional 10 days of postnatal ethanol exposure. Alterations in photoreceptors and other cells of the distal retina probably contributed to these deficits. The relevance and applicability of these data to FAS and subclinical alcohol embryopathy have yet to be demonstrated; however, they suggest that similar retinal alterations may occur in human FAS.

Prenatal ethanol exposure alters scotopic and photopic components of adult rat electroretinograms.

Cerebral oxidative metabolism in fetal sheep with multiple-dose ethanol infusion.

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Cerebral oxidative metabolism in fetal sheep with multiple-dose ethanol infusion.