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.