Failure of neurotransmitter blockers to alter PGE2-induced LH release.

The purpose of this study is to ascertain whether or not prostaglandin (PG) E2 induces LH release by modifying or modulating the release or action of neural transmitters. PGE2 injected iv into spayed rats primed two days earlier with 10 microgram estradiol benzoate increased the plasma levels of LH 10 min later as measured by radioimmunoassay. The peak of plasma LH was not changed by prior treatment with beta- or alpha-adrenergic receptor blockers, propranolol or phenoxybenzamine. The peak level of plasma LH did not alter in rats treated with DL-alpha-methyl-p-tyrosine methyl ester HCl (alpha-MPT) or sodium diethyldithiocarbamate (DDC). Similarly, the peak of plasma LH was not changed by prior treatment with imipramine. Administration of PGE2 produced an increase in anterior pituitary and plasma, but not hypothalamic cyclic AMP concomitantly with the elevation in plasma LH. Although it is possible that the effect of PGE2 could be mediated by another transmitter system, as yet unknown, or that the effect of PGE2 on LH release could be mediated via the adenylate cyclase-cyclic AMP system, the results indicate that PGE2 does not act trans-synaptically, but probably acts directly on LH-RH neurons.