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Effects of hypoxia‐ischemia on monoamine metabolism in the immature brain
Author(s) -
Silverstein Faye,
Johnston Michael V.
Publication year - 1984
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.410150407
Subject(s) - homovanillic acid , ischemia , hypoxia (environmental) , medicine , endocrinology , monoamine neurotransmitter , dopamine , striatum , brain ischemia , biology , chemistry , oxygen , serotonin , receptor , organic chemistry
We measured acute changes in monoamine metabolites in corpus striatum of immature rat pups exposed to hypoxiaischemia, hypoxia alone, or total global ischemia. Carotid ligations and two hours of 8% oxygen environment in 7‐day‐old pups led to asymmetrical turning behavior, a 70% decrease in endogenous striatal dopamine levels, and a 125% increase in homovanillic acid (HVA) concentrations on the side of ligation. In contrast, hypoxia alone and total global ischemia alone were not associated with HVA level elevation. Elevation of HVA level with hypoxia‐ischemia showed a threshold effect between 1 and 1.5 hours, and this time course paralleled that for production of gross morphological changes in rats raised to maturity. The data suggest that dopamine release from striatal nerve terminals is associated with events causing brain injury during perinatal hypoxia‐ischemia. Tissue HVA in the animal model appears to be a quantitative marker for the effects of the insult on a population of nerve terminals.