Fetal Alcohol Syndrome Research Today is a free monthly online journal that collates and summarizes the latest research about Fetal Alcohol Syndrome, including details on pregnancy, birth defects, causes, symptoms, treatment.

Paradoxical effect of ethanol on potassium channel currents and cell survival in cerebellar granule neurons.

Lefebvre T, Gonzalez BJ, Vaudry D, Desrues L, Falluel-Morel A, Aubert N, Fournier A, Tonon MC, Vaudry H, Castel H

Inserm U413, Laboratory of Neuroendocrine and Neuronal Cell Differentiation and Communication, European Institute for Peptide Research (IFRMP 23), University of Rouen, Mont-Saint-Aignan, France.

Abstract Transient exposure to ethanol (EtOH) results in a massive neurodegeneration in the developing brain leading to behavioral and cognitive deficits observed in fetal alcohol syndrome. There is now compelling evidence that K(+) channels play an important role in the control of programmed cell death. The aim of the present work was to investigate the involvement of K(+) channels in the EtOH-induced cerebellar granule cell death and/or survival. At low and high concentrations, EtOH evoked membrane depolarization and hyperpolarization, respectively. Bath perfusion of EtOH (10 mM) depressed the I(A) (transient K(+) current) potassium current whereas EtOH (400 mM) provoked a marked potentiation of the specific I(K) (delayed rectifier K(+) current) current. Pipette dialysis with GTPgammaS or GDPbetaS did not modify the effects of EtOH (400 mM) on both membrane potential and I(K) current. In contrast, the reversible depolarization and slowly recovering inhibition of I(A) induced by EtOH (10 mM) became irreversible in the presence of GTPgammaS. EtOH (400 mM) induced prodeath responses whereas EtOH (10 mM) and K(+) channel blockers promoted cell survival. Altogether, these results indicate that in cerebellar granule cells, EtOH mediates a dual effect on K(+) currents partly involved in the control of granule cell death.

Published 29 June 2009 in J Neurochem.
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Articles on Fetal Alcohol Syndrome published 25 June 2009:

Gender differences in the motivational processing of babies are determined by their facial attractiveness.   PLoS One, 4(6): e6042.

BACKGROUND: This study sought to determine how esthetic appearance of babies may affect their motivational processing by the adults. METHODOLOGY AND PRINCIPAL FINDINGS: Healthy men and women were administered two laboratory-based tasks: a) key pressing to change the viewing time of normal-looking babies and of those with abnormal facial features (e.g., cleft palate, strabismus, skin disorders, Down's syndrome and fetal alcohol syndrome) and b) attractiveness ratings of these images. Exposure to ... [Abstract] [Full-text]

Articles on Fetal Alcohol Syndrome published 22 June 2009:

Executive function deficits in children with fetal alcohol spectrum disorders (FASD) measured using the Cambridge Neuropsychological Tests Automated Battery (CANTAB).   J Child Psychol Psychiatry, 50(6): 688-97.

BACKGROUND: Chronic prenatal alcohol exposure causes a spectrum of deleterious effects in offspring, collectively termed fetal alcohol spectrum disorders (FASD), and deficits in executive function are prevalent in FASD. The goal of this research was to test the hypothesis that children with FASD exhibit performance deficits in tasks that assess attention, planning and spatial working memory. METHODS: Subjects (8-15 years male and female children) with a diagnosis of fetal alcohol syndrome ... [Abstract] [Full-text]

Articles on Fetal Alcohol Syndrome published 12 June 2009:

Prenatal Alcohol Exposure and Interhemispheric Transfer of Tactile Information: Detroit and Cape Town Findings.   Alcohol Clin Exp Res.

Background: Previous research has demonstrated that heavy prenatal alcohol exposure affects the size and shape of the corpus callosum (CC) and compromises interhemispheric transfer of information. The aim of this study was to confirm the previous reports of poorer performance on a finger localization test (FLT) of interhemispheric transfer in a cohort of heavily exposed children and to extend these findings to a cohort of moderately exposed young adults. Methods: In Study 1, the FLT was ... [Abstract] [Full-text]

Articles on Fetal Alcohol Syndrome published 11 June 2009:

Maternal age-specific risk of non-chromosomal anomalies.   BJOG, 116(8): 1111-9.

OBJECTIVES: To determine the excess risk of non-chromosomal congenital anomaly (NCA) among teenage mothers and older mothers. DESIGN AND SETTING: Population-based prevalence study using data from EUROCAT congenital anomaly registers in 23 regions of Europe in 15 countries, covering a total of 1.75 million births from 2000 to 2004. PARTICIPANTS: A total of 38,958 cases of NCA that were live births, fetal deaths with gestational age > or = 20 weeks or terminations of pregnancy following ... [Abstract] [Full-text]

Articles on Fetal Alcohol Syndrome published 9 June 2009:

GSK3beta in Ethanol Neurotoxicity.   Mol Neurobiol.

Alcohol consumption during pregnancy is a significant public health problem and may result in a wide range of adverse outcomes for the child. The developing central nervous system (CNS) is particularly susceptible to ethanol toxicity. Children with fetal alcohol spectrum disorders (FASD) have a variety of cognitive, behavioral, and neurological impairments. FASD currently represents the leading cause of mental retardation in North America ahead of Down syndrome and cerebral palsy. Ethanol ... [Abstract] [Full-text]

Multisite neuroimaging trials.   Curr Opin Neurol.

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Articles on Fetal Alcohol Syndrome published 4 June 2009:

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Articles on Fetal Alcohol Syndrome published 21 May 2009:

ETHANOL INHIBITS L1 CELL ADHESION MOLECULE TYROSINE PHOSPHORYLATION AND DEPHOSPHORYLATION AND ACTIVATION OF PP60.   J Neurochem.

ABSTRACT Fetal alcohol syndrome is a leading cause of mental retardation. The neuropathology found in patients with fetal alcohol syndrome overlaps with those with mutations in the gene for L1 cell adhesion molecule. We have previously shown that L1 mediated neurite outgrowth and L1 activation of ERK1/2 are inhibited at low concentrations of ethanol. One possible mechanism for this effect is through disruption of a tyrosine based sorting signal, Y(1176)RSLE, on the cytoplasmic domain of L1. Our ... [Abstract] [Full-text]

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