Dopamine stimulates the degradation of gonadotropin releasing hormone by rat synaptosomes.
Immunohistochemical studies have shown the existence of synapses between nerve endings containing dopamine and gonadotropin releasing hormone (LH-RH) respectively in the hypothalamic median eminence. It is generally accepted that this transmitter is involved in the regulation of gonadotropin secretion as a modulator of LH-RH release, although the evidence is conflicting and both inhibitory and excitatory actions of dopamine have been reported. In vitro studies support the excitatory effect and low doses of dopamine have been shown to release LH-RH from incubated hypothalamic fragments and synaptosomes. This report describes studies with nerve endings isolated from the rat hypothalamus in which dopamine at higher concentrations than those used previously has been found to stimulate the degradation of LH-RH but not thyrotropin releasing hormone (TRH). This mechanism seems to be physiological in that it is calcium-dependent, requires the structural integrity of the nerve endings and fluctuates with the reproductive state of the animal.
D000818:Animals; D002118:Calcium / Q000494:pharmacology; D002540:Cerebral Cortex / Q000187:drug effects; D004298:Dopamine / Q000494:pharmacology*; D004971:Estrus; D005260:Female; D007987:Gonadotropin-Releasing Hormone / Q000378:metabolism*; D007031:Hypothalamus / Q000378:metabolism*; D008297:Male; D009411:Nerve Endings / Q000187:drug effects; D011247:Pregnancy; D051381:Rats; D012737:Sex Factors; D013574:Synaptosomes / Q000378:metabolism*; D013973:Thyrotropin-Releasing Hormone / Q000378:metabolism
D007987:Gonadotropin-Releasing Hormone; D013973:Thyrotropin-Releasing Hormone; D002118:Calcium; D004298:Dopamine