title: Maternal ethanol consumption: binding of L-glutamate to synaptic membranes from whole brain, cortices, and cerebella of offspring.
abstract: We examined the influence of chronic maternal ethanol consumption on the Na+- and Ca2+-independent binding of L-glutamate to synaptic plasma membranes from whole brain as well as from cortices and cerebella of developing offspring. The maximum specific binding (Bmax) of L-glutamate to the Na+- and Ca2+-independent binding sites in synaptic plasma membranes of brain peaked at 17 days of age in the offspring of both control and ethanol-fed rats, although at that age there were significantly fewer binding sites in the brains of the offspring of ethanol-fed rats. The regional localization of this deficit is not now known. However, it appears that one major glutamatergic region (the cortex) does not reflect the transient deficiency of L-glutamate sites in brain. In fact, the concentration of L-glutamate binding sites in cortical synaptic plasma membranes was significantly increased in the 20-day-old offspring of ethanol-fed rats. In contrast to the cortex, binding to cerebellar synaptic plasma membranes was comparable in 20-day-old offspring of control and ethanol-fed rats. Despite transient alterations in the concentrations of L-glutamate binding sites in brain and synaptic plasma membranes, the affinity of the sites for L-glutamate (Kd) was consistently normal in the 14- to 26-day-old offspring of ethanol-fed rats.
mesh_terms: D000428:Alcohol Drinking; D000818:Animals; D000831:Animals, Newborn / Q000378:metabolism*; D001665:Binding Sites; D001921:Brain / Q000378:metabolism*; D002531:Cerebellum / Q000378:metabolism*; D002540:Cerebral Cortex / Q000378:metabolism*; D005260:Female; D005971:Glutamates / Q000378:metabolism*; D011247:Pregnancy; D051381:Rats; D011919:Rats, Inbred Strains; D013570:Synaptic Membranes / Q000378:metabolism*; D014018:Tissue Distribution
chemical_list: D005971:Glutamates