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L-3,4-Dihydroxyphenylalanine (L-Dopa) as an Inhibitor of Prolactin Release*
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1978
Year
NeuroendocrinologyPharmacotherapyFemale Reproductive FunctionProlactin ReleaseAnterior PituitaryReproductive EndocrinologyMolecular PharmacologyHypothalamic PeptideReproductive MedicinePublic HealthBiochemistryEndocrine MechanismMedicineMechanism Of ActionNeuropharmacologyEndocrinologyPharmacologyPhysiologyUterine ReceptivityMk 486Endocrine Research
A series of experiments was performed on estrogen/progesterone-treated, ovariectomized rats to determine the site of the inhibitory effect of L-3,4- dihydroxyphenylalanine (L-dopa) on prolactin release. After intraarterial injection of L-[3H]dopa (150 μCi), [3H]norepinephrine ([3H]NE), [3H]dopamine ([3H]DA), and L-[3H]dopa were found in the hypothalamus and anterior pituitary. Intra-arterial injection of L-dopa (2, 5, or 10 mg/kg) produced a dose-related inhibition of prolactin release. The magnitude and the duration of inhibition of prolactin release were greater with increasing doses of L-dopa. Hypothalamic concentrations of endogenous DA were significantly increased 30 min after L-dopa (10 mg/kg) and were correlated with decreased serum prolactin levels at this time. Hypothalamic NE content was not affected. L-α-Methyldopa hydrazine, 20 mg/kg (Mk 486), a peripheral aromatic L-amino acid decarboxylase inhibitor, injected 30 min before L-[3H]dopa injection, increased the concentration of L-[3H]dopa in the hypothalamus and anterior pituitary, decreased the concentration of [3H]NE and [3H]- DA in the submaxillary gland (a representative, adrenergically innervated peripheral tissue), and increased the concentration of [3H]NE and [3H]DA in the hypothalamus compared to controls. Although L-[3H]dopa concentration in the anterior pituitary was increased, [3H]NE and [3H]DA concentrations did not show similar increases. Mk 486 (20, 30, or 40 mg/kg) alone produced a significant increase in plasma prolactin concentration 35 min after injection. L-Dopa, 5 mg/kg, effectively inhibited prolactin release in animals pretreated with Mk 486; however, the effect of L-dopa was attenuated 5–10 min after injection and enhanced 15–30 min compared to the effect obtained with L-dopa alone. Plasma LH levels were not affected by Mk 486 and/or L-dopa. The delayed onset of the inhibition of prolactin release by L-dopa when its conversion to DA was blocked in the periphery suggests that L-dopa entered the brain and was converted to DA before it was effective. In addition, the increase in prolactin levels after injection of Mk 486 alone suggests that peripheral DA tonically inhibits prolactin release. (Endocrinology102: 166, 1978)