Failure of Neurotransmitter Blockers to Alter PGE₂-Induced LH Release

抄録

The purpose of this study is to ascertain whether or not prostaglandin (PG) E₂induces LH release by modifying or modulating the release or action of neural transmitters.
PGE₂injected iv into spayed rats primed two days earlier with 10βg estradiol benzoate increased the plasma levels of LH 10 min later as measured by radio-immunoassay. The peak of plasma LH was not changed by prior treatment with βorα-adrenergic receptor blockers, propranolol or phenoxybenzamine. The peak level of plasma LH did not alter in rats treated with DL-α-methyl-p-tyrosine methyl ester HCI (α-MPT) or sodium diethyldithiocarbamate (DDC). Similarly, the peak of plasma LH was not changed by prior treatment with imipramine. Administration of PGE₂produced an increase in anlerior pituitary and plasma, but not hypothalamic cyclic AMP concomitantly with the elevation in plasma LH.
Although it is possible that the effect of PGE₂could be mediated by another transmitter system, as yet unknown, or that the effect of PGE₂on LH release could be mediated via the adenylate cyclase-cyclic AMP system, the results indicate that PGE₂does not act trans-synaptically, but probably acts directly on LH-RH neurons.