Abstract
MUCH work has been directed at demonstrating the possible interaction of ethanol with levels of neurotransmitter amines or their metabolism in brain1,2. We have previously demonstrated an increase in brain levels of 5-hydroxyindoleacetic acid (5-HIAA) in mice after both a single and chronic administration of ethanol3. Our more recent work4 has focused attention on the inhibition of transport of 5-HIAA from the central nervous system (CNS) by ethanol as the factor responsible for the increase in brain 5-HIAA after ethanol. 5-HIAA diffuses from the CNS into cerebrospinal fluid (CSF), from which it is removed by a carrier-mediated transport into the bloodstream5. The effect of ethanol on transport of 5-HIAA from CSF was studied by perfusing this acid through the spinal subarachnoid space from the cisterna magna to the lumbar region of cats. This was shown to be a sensitive and reliable model for the study of transport of 5-HIAA from CSF (ref. 6).
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TABAKOFF, B., BULAT, M. & ANDERSON, R. Ethanol inhibition of transport of 5-hydroxyindoleacetic acid from cerebrospinal fluid. Nature 254, 708–710 (1975). https://doi.org/10.1038/254708a0
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DOI: https://doi.org/10.1038/254708a0
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