We have assessed the effects on LH release of prolonged naloxone (NAL) treatment before the critical period on proestrus. When LH secretion was monitored at 5-min intervals immediately after the start of continuous NAL infusion (2 mg/0.6 ml saline X h iv) at 1000 h, two types of responses were observed. In three of six rats, a small increase (1-2 ng rat LHRH-2/ml) during the first hour was followed by a sharp rise to 4-5 ng/ml in the second hour and a gradual return to baseline levels (0.5-1.00 ng/ml) in the third hour of infusion. In the remaining rats, LH responses were small with peak levels reaching 2 ng/ml range. When the effects were monitored 1 h after starting NAL infusion at 1000 h, the LH response was improved. Peak LH levels observed shortly before or after 1200 h varied between 4-14 ng/ml and in some rats the levels were comparable to those seen normally in the afternoon of proestrus (9-24 ng/ml). However, delaying the start of NAL infusion to 1200 h produced LH surges before 1400 h, with peak levels (27.5 +/- 5.5 ng/ml) in the range of normal preovulatory LH surges (peak levels 16.6 +/- 2.5 ng/ml), followed by a steady decrease in LH secretion. Additionally, sc NAL pellets implanted at 0930 h provoked premature LH hypersecretion with a temporal pattern (0930-1430 h) and magnitude (peak levels, 26.3 +/- 4.3 ng/ml between 1100-1200 h) comparable to the normal preovulatory LH surge observed after 1330 h. Since NAL is believed to antagonize the inhibitory effects of endogenous opioids on LH secretion, the results of this study imply that a sustained restraint on this inhibitory opioid tone can elicit the LH surge before the critical period on proestrus. These findings are in accord with our thesis that the neural clock that normally triggers the preovulatory LH surge may transiently decrease the inhibitory opioid tone to allow expression of crucial neural events which culminate in preovulatory LH secretion.
Intraventricular injection of neuropeptide Y (NPY) stimulates LH release in estradiol benzoate- and progesterone-primed (EBP) ovariectomized rats. Because adrenergic neurotransmitters, norepinephrine (NE) and epinephrine (E), show intraneuronal coexistence with NPY in certain brain regions of the rat and there are similarities in the effects of NPY and NE/E on LH release, we investigated the possible interaction of NPY and adrenergic receptor systems in the stimulation of LH release in EBP-treated ovariectomized rats. The experiments were designed to determine whether NPY exerted its effects via adrenergic receptors and whether combined administrations of NPY and NE can act synergistically or in an additive manner to enhance the LH release response. Permanent stainless steel cannulae were placed in the third ventricle of the brain, and the rats were ovariectomized. Two weeks after surgery, rats were injected with EB (30 micrograms/rat) and P (15 mg/rat). Two days later, the effects of either vehicle alone (control) or various adrenergic and dopaminergic receptor antagonists and an opiate receptor agonist on stimulation of LH release by NPY were assessed. Intraventricular injection of 0.47 nmol NPY increased plasma LH levels at 10, 20, and 30 min in control rats. The NPY-induced LH response was not blocked by pretreatment with any of the following drugs: the alpha-adrenoreceptor antagonist phenoxybenzamine, the alpha 1-adrenoreceptor antagonist prazosin, beta-adrenoreceptor antagonist propranolol, the dopamine receptor antagonist pimozide, or the opiate receptor agonist morphine. All of these drugs affect LH release in other circumstances. On the other hand, the alpha 2-adrenoreceptor antagonist yohimbine significantly attenuated the NPY-induced LH increments. In the second study dealing with the possible synergistic or additive interactions between NPY and NE, we observed that when doses of NPY and NE that separately were only minimally effective in stimulating LH release were administered together, the amounts of LH secreted were greater than the sum of the individual responses. However, when NE and NPY were given together in doses that alone had either no stimulatory or maximal stimulatory effects, there were no additive or synergistic effects on LH release.(ABSTRACT TRUNCATED AT 400 WORDS)
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