Development of histaminergic pathways in brain as influenced by maternal alcoholism.
The development of histaminergic pathways has been studied in the rat brain specially as influenced by maternal alcoholism. Maternal ethanol consumption during pregnancy results in an increase in the cerebral histamine levels of the fetus. An increase in the brain histamine levels is also observed in the newborn rats suckling on the ethanol-fed mothers compared to the corresponding controls. Brain histamine levels are highest towards latter part of the pregnancy and lowest in the adult brains, whereas the brain histidine decarboxylase activity is lowest in the fetal brains and highest in the adult brains. Maternal alcoholism either during gestation or during lactation did not significantly affect histidine decarboxylase activity in the fetal and neonatal brains. Acute administration of ethanol or acetaldehyde after 20 minutes resulted in significant increase in the brain histamine levels. This increase in the brain histamine levels seems to be a direct result of brain histamine release due to ethanol or acetaldehyde metabolism in the body. The effect of ethanol on brain histamine levels may have important implications inview of the fact that both histamine and ethanol influence diuresis, EEG activity, and thermoregulation in the body.
D000079:Acetaldehyde / Q000494:pharmacology; D000437:Alcoholism / Q000503:physiopathology*; D000818:Animals; D001921:Brain / Q000196:embryology / Q000254:growth & development*; D001923:Brain Chemistry / Q000187:drug effects; D005260:Female; D006632:Histamine / Q000378:metabolism / Q000502:physiology*; D006640:Histidine Decarboxylase / Q000378:metabolism; D006801:Humans; D007774:Lactation; D009434:Neural Pathways / Q000196:embryology / Q000254:growth & development*; D011247:Pregnancy; D051381:Rats
D006632:Histamine; D006640:Histidine Decarboxylase; D000079:Acetaldehyde