Receptor blocking drugs were used to determine whether adrenergic, dopaminergic, serotoninergic, or cholinergic synapses are involved in mediating the LH release induced by intraventricularly injected PGE2. Prostaglandin E2 (5 âµg) was injected into the 3rd ventricle (3rd V) of ovariectomized rats, and plasma LH concentrations before and after treatment were determined by radioimmunoassay. Phentolamine, 20 or 30 âµg, or pronethalol, 20 âµg (Î± andâµ adrenergic receptor blockers, respectively) injected into the 3rd V failed to alter the elevation of plasma LH evoked by PGE2 injected into the ventricle 10 min later. Likewise, LH release following PGE2 was not changed when a dopaminergic blocker, pimozide (0.63 mgâ kg, SC), was injected 2 h prior to PGE2. Two antagonists of serotonin, methysergide maleate (3 mgâ kg, ip) orcinanserin HC1 (1 mgâ kg, iv) given 2h or 45 min before PGE2 respectively, failed to alter the action of PGE2. Atropine(100or250âµg) injected into the 3rd V 10 min prior toPGE2 was also ineffective in blocking the increase in plasma LH following PGE2. The results of this study indicate that the effect of PGE2 on LH release is not mediated by adrenergic, dopaminergic, serotoninergic, or cholinergic receptors. They also suggest that PGE2 is not acting trans-synaptically but probably directly on the LHRH neuron to induce the discharge of LHRH into the hypophysial portal vessels which then evokes release of LH from the adenohypophysis.
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