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EFFECTS OF INGESTION OF A CARBOHYDRATE‐FAT MEAL ON THE LEVELS AND SYNTHESIS OF 5‐HYDROXYINDOLES IN VARIOUS REGIONS OF THE RAT CENTRAL NERVOUS SYSTEM
Author(s) -
Colmenares J. L.,
Wurtman R. J.,
Fernstrom J. D.
Publication year - 1975
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1975.tb04413.x
Subject(s) - serotonin , tryptophan , medicine , endocrinology , ingestion , striatum , hypothalamus , neurotransmitter , decarboxylase inhibitor , central nervous system , meal , biology , carbohydrate , monoamine neurotransmitter , in vivo , 5 hydroxyindoleacetic acid , chemistry , dopamine , biochemistry , amino acid , levodopa , receptor , disease , parkinson's disease , microbiology and biotechnology
—The concentrations of tryptophan, serotonin (5‐HT), and 5‐hydroxyindoleacetic acid (5‐HIAA) in spinal cord and most brain regions increase 2 h after fasted rats begin to consume a carbohydrate‐fat meal: indole levels rise in all portions of the brain studied, but the increase is not statistically significant in the hypothalamus and corpus striatum. The rate at which the brain synthesizes 5‐hydroxy‐indoles (as estimated in vivo by measuring 5‐hydroxytryptophan accumulation following an injection of the decarboxylase inhibitor RO4‐4602) is also accelerated in all of the regions in which the experimental diet elevates tryptophan, 5‐HT and 5‐HIAA levels. These observations indicate that the previously reported increase in brain 5‐hydroxyindole levels following consumption of a protein‐free meal reflects accelerated serotonin synthesis, and occurs within both the cell bodies and the terminals of serotonin‐containing neurons. It is possible that diet‐induced changes in neuronal serotonin levels influence the quantities of the neurotransmitter released into synapses, either spontaneously or in response to drugs.