Further Studies on Dopamine-Induced Suppression of Pulsatile LH Release in Ovariectomized Rats

Abstract

Third ventricular administration of dopamine (DA) in ovariectomized rats suppresses pulsatile LH secretion in a dose-dependent manner (Neuroendocrinology 29: 149, 1979). Since infusion of norepinephrine (NE) also produces a similar response, and DA can be taken up by noradrenergic fibers and converted to NE, an experiment was carried out to determine whether DA acted by directly activating DA receptors. This study also examined which parameters of pulsatile LH secretion were affected during DA-induced suppression of this release process, i.e., the LH interpulse interval and/or the magnitude of increase in blood LH levels produced by LH pulses. Infusion of DA in control rats pretreated with tartaric acid or /-butaclamol decreased mean blood LH levels. This effect is due entirely to a marked increase in the LH interpulse interval, since no change was seen in the magnitude of increase in blood LH levels produced by those LH pulses that did occur during DA infusion. Blockade of DA receptors with pimozide prevented the decrease in blood LH levels in response to DA and significantly reduced the change in the LH interpulse interval. These data indicate that DA suppresses pulsatile LH release solely by affecting the periodicity of this rhythm, and that this effect is mediated primarily through an activation of DA receptors. Pretreatment with d-butaclamol, another DA receptor antagonist, had no effect on the response to DA. As in control rats, DA-induced suppression of pulsatile LH release was again due entirely to a lengthening of the LH interpulse interval. d-Butaclamol does block the inhibition of pulsatile LH release due to peripheral administration of the DA receptor agonist, apomorphine (Endocrinology 100: 796, 1977). However, when concentrations of apomorphine equimolar to DA were infused into the third ventricle in d- or l-butaclamol-treated rats, comparable suppressions of pulsatile LH release occurred. This suggests that the failure of d-butaclamol to prevent the suppression of pulsatile LH release by intraventricular DA administration was apparently due to an ineffective level of DA receptor blockade.

Physiological role of alpha-melanocyte-stimulating hormone in modulating the secretion of prolactin and luteinizing hormone in the female rat.

“…The regulation of pulsatile secretion of LH is complex and involves a number of neurotransmitters. Dopamine is thought by some investigators (21) to stimulate the secretion of LH, whereas others have provided evidence supporting an inhibitory effect (22,23). Gallo (22) has provided evidence that dopamine decreases the frequency of LH pulses.…”

“…Dopamine is thought by some investigators (21) to stimulate the secretion of LH, whereas others have provided evidence supporting an inhibitory effect (22,23). Gallo (22) has provided evidence that dopamine decreases the frequency of LH pulses. If a-MSH-induced inhibition of LH is mediated by dopamine, as postulated earlier by us (9), it is unclear why the intraventricular injection of anti-MSH did not alter the frequency of LH pulses.…”

Prolactin Suppresses GnRH but Not TSH Secretion

“…The increased dopamine turnover occurs within 2 h [4] . Both increased prolactin [45,46] and dopamine [22,28] suppress TSH secretion and, less consistently, LH and GnRH secretion in animals, suggesting that prolactin's suppressive effects on GnRH and TSH may be mediated by dopamine. In women in the current study, however, r-hPRL administration producing prolactin levels consistent with those in the early postpartum [32][33][34][35] and in women with prolactinomas [36] induced suppression of LH, and therefore GnRH pulse frequency [47,48] , but did not affect TSH secretion after 7 days.…”

“…Further, increasing prolactin levels in normal women for up to 24 h using a dopamine antagonist did not decrease LH pulse frequency [18,19] . Finally, although dopamine modestly inhibits GnRH release in rodent models [20][21][22] , in healthy humans dopamine infusions have caused variable changes in gonadotropin release [23,24] and an increase in LH in hyperprolactinemic subjects [23] . Taken together, the degree to which prolactin suppresses GnRH and the mechanism for this potential GnRH suppression in the human is not clear.…”

Neuroendocrine control of ovarian function in the primate

“…Dopamine, administered peripherally, has been shown to inhibit LH secretion in agonadal women (Judd, Rigg & Yen, 1979). Intraventricularly administered dopamine in the rat suppresses LH by a decrease in the frequency of the pulsatile LH discharge, pulse amplitude remaining unchanged (Gallo, 1981). The effects of other biogenic amines and neurotransmitters remain to be investigated in the primate.…”