Reversal ofβ-Endorphin-Induced Blockade of Ovulation and Luteinizing Hormone Surge with Prostaglandin E2*

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Abstract
The effects of intraventricular (Ivt) administration of .beta.-endorphin (.beta.E) on preovulatory LH [luteinizing hormone] release, ovulation and the mechanism that may be involved in opioid action were examined. Female rats were implanted with permanent cannulae in the third ventricle of the brain and were allowed to recover 4-day estrous cyclicity. Intrajugular cannulae were placed on the morning of proestrus. Thereafter, they received Ivt either saline (2 .mu.l) or .beta.E (10 .mu.g/2 .mu.l) at 1300, 1430 and 1600 h. In addition, at 1600, 1700 and 1800 h, they were injected Ivt with either vehicle (CSF or saline) or 1 of the following compounds: epinephrine (15.3 .mu.g), norepinephrine (15.3 .mu.g) or prostaglandin E2 (6 .mu.g). Blood samples for LH measurements were taken, 0, 10, 30 and 60 min after the additional injections at 1600 and 1700 h. .beta.E blocked the preovulatory LH surge and ovulation. Administration of the opiate receptor antagonist naloxone (2 mg/kg) reversed these effects. Epinephrine stimulated a small discharge of LH only after 2nd E injection in the .beta.E-treated rats, but this was insufficient to restore ovulation. Prostaglandin E2 reversed the .beta.E blockade of the LH surge and ovulation. Apparently, .beta.E blocks ovulation and the LH surge primarily by suppressing either the influx or adrenergic expression of the spontaneous neurogenic stimuli responsible for the preovulatory LH discharge and not by evoking a general decrease in secretory response of the LHRH neurons.

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