Maternal alcohol ingestion and neural tube defects

Castro-Gago, Manuel; Rodriguez-Cervilla, J.; Ugarte, J.; Novo, I.; Pombo, Marta

doi:10.1016/s0022-3476(84)80973-7

Cited by 11 publications

(4 citation statements)

References 3 publications

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“…[42][43][44][45][46][47] In addition to the 4 postmortem cases of holoprosencephaly-arhinencephaly noted above, 2 additional cases have been confirmed with ultrasound, and a seventh case with cyclopia and presumed alobar holoprosencephaly was reported although not confirmed. 27,29,[33][34][35] In general, craniofacial anomalies, such as those described in patients with FAS, have often been associated with abnormalities of brain development.…”

Section: Neuropathologic Studiesmentioning

confidence: 99%

Magnetic Resonance Imaging of Brain Anomalies in Fetal Alcohol Syndrome

et al. 1997

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Patients with classic FAS have a high incidence of midline brain anomalies. This finding is consistent with the concept that the midline CNS is a developmental field that is particularly susceptible to the teratogenic effects of alcohol. Furthermore, patients with more severe facial dysmorphologic characteristics are more likely to have midline brain anomalies. In addition, we observed a high incidence of micrencephaly with a wide range of severity.

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Section: Neuropathologic Studiesmentioning

confidence: 99%

Magnetic Resonance Imaging of Brain Anomalies in Fetal Alcohol Syndrome

et al. 1997

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“…However, the mechanisms by which in utero alcohol exposure adversely affects fetal brain development and function are largely unknown. Although fetal alcohol exposure has been linked to neural tube defects [3] as well as disruptions in the development of neural pathways [4,5] , it may also induce vascular abnormalities and dysfunction [6][7][8][9] . Because brain perfusion is tightly coupled to neuronal activity [10] , alterations in cerebrovascular development may contribute to the deleterious effects of alcohol exposure on the developing brain.…”

Section: Introductionmentioning

confidence: 99%

Fetal Alcohol Exposure Alters Cerebrovascular Reactivity to Vasoactive Intestinal Peptide in Adult Sheep

et al. 2007

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Chronic fetal alcohol exposure impairs neural and vascular development. We have previously shown that fetal alcohol exposure is associated with attenuated hypoxic cerebral vasodilation and reduced neuronal vasoactive intestinal peptide (VIP) expression in fetal sheep. In the present study, we tested the hypothesis that fetal alcohol exposure alters vascular development, leading to altered cerebral vascular reactivity to VIP in adulthood. Penetrating intracerebral arterioles were harvested from the brains of adult (10–13 months old) offspring of ewes that had received intravenous infusions of alcohol (1.5 g/kg) or same-volume saline (90 min/day, 5 days/week) during days 30–82 of gestation (full term = 145 days). The isolated arterioles were cannulated with a micropipette system that allowed luminal perfusion and control of luminal pressure and developed spontaneous tone at 40°C and 60 mm Hg luminal pressure. There was no difference in myogenic tone between arterioles exposed prenatally to alcohol (n = 18) and saline controls (n = 17). However, fetal alcohol exposure significantly (p = 0.03) enhanced the dilator responses of adult intracerebral arterioles to VIP [0.1 nM to 1 µM, logEC₅₀: –8.6 ± 0.2 (alcohol) vs. –7.4 ± 0.8 (saline)]. In contrast, there was no difference in dilator responses to H⁺ (pH 6.8 buffer), to adenosine (10 nM to 0.1 mM), or to CGS21680 (an adenosine A_2A receptor agonist, 0.01 nM to 10 µM). Thus, fetal alcohol exposure alters vasomotor sensitivity to VIP in adult intracerebral arterioles – perhaps a compensatory response to alcohol-induced underdevelopment of neurotransmitter pathways involved in cerebral vascular regulation.

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“…Although neural tube closure defects (especially anencephaly) are not considered typical of the pattern of human alcohol-related major malformations, several reports relate alcohol abuse in the fi rst month of pregnancy to subsequent neural tube defects (NTDs) [Friedman, 1982;Castro-Gago et al, 1984]. Animal studies support the hypothesis that alcohol induces NTDs [Chernoff, 1977;Randall and Taylor, 1979;Webster et al, 1980;Sulik et al, 1981;Kotch et al, 1995].…”

Section: Introductionmentioning

confidence: 99%

Peptide-Mediated Protection from Ethanol-Induced Neural Tube Defects

et al. 2005

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Ethanol inhibition of L1-mediated cell adhesion may contribute to the spectrum of neurological, behavioral and morphological abnormalities associated with prenatal ethanol exposure. We showed previously that the neuroprotective peptides NAPVSIPQ (NAP) and SALLRSIPA (SAL) antagonize ethanol inhibition of L1 adhesion and prevent ethanol-induced growth retardation in mouse whole embryo culture. Here we ask whether NAP and SAL also prevent ethanol-induced major malformations of the nervous system. Gestational day 8.0 (3–5 somites) C57BL/6J mouse embryos were grown for 6 h in control medium, 100 mM ethanol and 10^–10M peptides and then maintained for an additional 20 h in control medium. At the end of the culture period, only embryos having 18–19 somite pairs were examined and compared for the degree of neural tube closure. Ethanol exposure resulted in neural tube defects (NTDs) consistent with total dysraphia and anencephaly. Co-incubation with ethanol and L-NAP (all L-amino acids), D-NAP (all D-amino acids) or SAL significantly increased the percentage of embryos that had begun to close their neural folds at the level of the forebrain/midbrain junction or that had progressed beyond this stage of closure. P7A-NAP (NAPVSIAQ), which lacks neuroprotective activity, but retains activity as an antagonist of ethanol inhibition of L1 adhesion, was effective in preventing ethanol-induced NTDs. In contrast, I6A-NAP (NAPVSAPQ), which shows reduced efficacy as an ethanol antagonist but retains its neuroprotective efficacy, did not significantly diminish the induction of NTDs by ethanol. These findings demonstrate the ability of NAP and SAL to prevent ethanol-induced NTDs and support the hypothesis that ethanol teratogenesis is caused in part by ethanol inhibition of L1-mediated cell adhesion.

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Maternal alcohol ingestion and neural tube defects

Cited by 11 publications

References 3 publications

Magnetic Resonance Imaging of Brain Anomalies in Fetal Alcohol Syndrome

Magnetic Resonance Imaging of Brain Anomalies in Fetal Alcohol Syndrome

Fetal Alcohol Exposure Alters Cerebrovascular Reactivity to Vasoactive Intestinal Peptide in Adult Sheep

Peptide-Mediated Protection from Ethanol-Induced Neural Tube Defects

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