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Possible Role of Dopamine as Transmitter To Promote Discharge of LH-Releasing Factor
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1969
Year
Lh ReleaseNeurotransmitterNeuroendocrinologyNeurotransmissionHypothalamic CircuitsSocial SciencesReproductive EndocrinologyPituitary GlandNeuroendocrine MechanismHypothalamic PeptidePossible RoleNeurochemistryAnimal PhysiologyPromote DischargeNeuropharmacologyNervous SystemEndocrinologyPharmacologyDopamineLh-releasing FactorNeurotransmitter SystemsDopamine ResearchNeurophysiologyPhysiologyNeuroendocrine DisorderEnhanced Lrf ReleaseNeuroscienceMedicineBasal Release
Recent evidence indicates the presence in the hypothalamus of neurons which contain dopamine (DA), norepinephrine (NE) and serotonin (5-HT). These in vitro experiments were performed to determine if any of these agents, or epinephrine (E), might play a role in the regulation of LH release. Doses of 0.5, 2.5 or 5.0 μg/ml of DA, NE or 5-HT failed to alter LH released from pituitaries incubated alone, whereas 5.0 μg/ml E enhanced LH release to some extent. DA at a 25.0 μg/ml dose significantly decreased assayable LH by inactivating it. When pituitaries were incubated in the presence of stalkmedian eminence (SME) tissue (2 SME/gland), LH release was stimulated by an average of 20.7% (p < .05). If the combined SME and pituitary tissue was incubated with 0.5–5.0 μg/ml of either NE or 5-HT, this basal release of LH was unaffected. LH release was significantly enhanced (p < .01) when DA was added to the incubation medium in doses of 0.5–5.0 μg/ml, and a dose response could be obtained. These results can only be explained by an enhanced LRF release by incubated hypothalamic tissue in the presence of DA, because DA in similar doses failed to potentiate the LH-releasing action of crude rat hypothalamic extracts or of purified ovine LRF. E in a 5.0 μg/ml dose caused some inhibitory action in the presence of SME fragments. It is suggested that hypothalamic dopaminergic neurons synapse with the neurosecretory neurons which secrete the LRF and stimulate its release. DA appears to act on α-adrenergic receptors to cause discharge of LRF since the response to DA was completely inhibited by phentolamine. The α-blocker failed to influence either basal or LRF-stimulated release of LH from pituitaries incubated alone. On the other hand, the β-blocker, pronethalol, had no inhibitory effect. Hypothalamic tissue of each sex had the same order of responsiveness to DA. (Endocrinology85: 121, 1969)