Alcohol intake during prenatal life affects neuroimmune mediators and brain neurogenesis.
Several lines of evidence suggest that alcohol exposure during prenatal gestation, or during early postnatal life may be a risk factor for the manifestation of neurological and for immune-related disorders in later life. The cellular, biochemical and molecular mechanisms of ethanol toxicity, however, have not been yet clearly established. Recent studies indicated that neurotrophin signaling pathways may be involved in ethanol mediated cell death. The present investigation addressed the question of whether nerve growth factor (NGF), which is the first and best characterized member of the neurotrophin family, and NGF-target cells are affected by prenatal exposure to alcohol. The result of our study indicates that NGF synthesis and the functional activity of NGF-target cells localized in the brain are markedly influenced by ethanol intake. The possible link between such changes and the hypothesis that these alterations may contribute to certain of the neuropathology observed following alcohol exposure would be discussed.
Aloe
Luigi
L
Istituto di Neurobiologia e Medicina Molecolare, Consiglio Nazionale delle Ricerche, Rome, Italy. luigi.aloe@inmm.cnr.it
D000818:Animals; D001921:Brain / Q000187:drug effects / Q000196:embryology*; D001923:Brain Chemistry / Q000187:drug effects; D002492:Central Nervous System Depressants / Q000633:toxicity*; D002795:Choline O-Acetyltransferase / Q000378:metabolism; D000431:Ethanol / Q000633:toxicity*; D005260:Female; D005333:Fetus / Q000187:drug effects*; D009414:Nerve Growth Factors / Q000378:metabolism; D015213:Neuroimmunomodulation / Q000187:drug effects*; D011247:Pregnancy; D051381:Rats; D017207:Rats, Sprague-Dawley; D013234:Stem Cells
D002492:Central Nervous System Depressants; D009414:Nerve Growth Factors; D000431:Ethanol; D002795:Choline O-Acetyltransferase