Abstract
In order to investigate whether the capacity of hypothalamic and anterior pituitary tissue to concentrate and retain estradiol is affected by serotonin (5-HT), 3H-estradiol (3HE2) retention in these structures was measured after 5-HT synthesis inhibition by either parachlorophenylalanine (PCPA) or 6-fluoro-tryptophane (6 FTrp), or after destruction of midbrain raphe nuclei containing 5-HT cell bodies, as well as after administration of the 5-HT precursor 5-hydroxytryptophane (5-HTP). No modification in 3HE2 retention was observed after tryptophane hydroxylase inhibitors of raphe lesions; administration of the precursor only increased the steroid retention at very high, nonphysiological dose levels. It is concluded that the interaction of 5-HT with gonadotropic release cannot be accounted for by a direct effect on specific estrogenic receptors, but occurs at a different level of gonadotropic release regulating structures or directly on LH-RH neurons.
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