Abstract
The striatum seems to be the main brain region involved in stereotyped behavior induced by dopaminergic agonists. Rapid eye movement (REM) sleep deprivation increases dopaminergic agonist-induced stereotypy and produces biochemical changes in striatal dopaminergic neurotransmission. However, the mechanism underlying the increased dopaminergic sensitivity induced by REM sleep deprivation has not been elucidated. In an attempt to determine some of the biochemical changes in striatal dopaminergic neurotransmission that could contribute to REM sleep deprivation effects, we measured the activity of monoamine oxidase (MAO) A and B, the enzymes responsible for dopamine and beta-phenylethylamine (beta-PEA) deamination in striatum. Male adult rats were deprived of REM sleep for 96 h by the flower-pot technique. MAO A and B were assayed radioisotopically in the mitochondrial fraction by standard laboratory procedures, using [ 14C]-5-hydroxytryptamine (5-HT) and [ 14C]-beta-phenylethylamine (beta-PEA), as substrates for MAO A and MAO B, respectively. The results showed no significant statistical differences in striatal MAO A activity, whereas a significant decrease in MAO B activity was observed. The results are discussed in terms of the possible involvement of beta-PEA, a striatal endogenous trace amine, which potentiates dopaminergic neurotransmission and may participate in the increased dopaminergic sensitivity observed after REM sleep deprivation.
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