Release of LH occurred in ovariectomized, oestrogen-primed rats when the medial preoptic area (mPOA) was electrically stimulated with monophasic square pulses of 1 ms duration (50 Hz, 150 μA, 15 s on and 15 s off for 30 min). Electrochemical stimulation of the anterior cingulate area applied immediately after the first 15 min period of stimulation in the mPOA completely prevented the rise in LH normally observed during the following 15 min. This effect was suppressed either by selective blockade of noradrenaline synthesis with diethyldithiocarbamate, or following systemic or intraventricular injection of the βadrenergic blocker, propranolol, whereas it did not change after systemic atropine, pimozide or phenoxybenzamine. Isoprenaline, a β-adrenergic agonist, injected into the third ventricle of rats stimulated in the mPOA mimicked the effect of the cortical stimulation, this effect was also blocked by propranolol. Intraventricular administration of propranolol or of isoprenaline had no effect on the release of LH induced by the injection of gonadotrophin releasing hormone, showing that their action is not directly on the pituitary gland. Intraventricular injection of noradrenaline, which failed to affect the release of LH induced by stimulation in the mPOA, inhibited this release when animals were pretreated with phenoxybenzamine. On the other hand, the LH-releasing potency of noradrenaline was greatly increased if the β-receptors were blocked.
From these results it may be concluded (1) that inhibition of the secretion of LH evoked by electrochemical stimulation of the anterior cingulate cortex is mediated by an adrenergic mechanism involving a β-receptor and (2) that noradrenaline exerts an inhibitory effect on the secretion of LH through a β-receptor in addition to the known facilitatory action through an α-receptor.
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