ROLE OF NEUROPEPTIDE-Y IN EPISODIC LUTEINIZING-HORMONE RELEASE IN OVARIECTOMIZED RATS - AN EXCITATORY COMPONENT AND OPIOID INVOLVEMENT

Citation
B. Xu et al., ROLE OF NEUROPEPTIDE-Y IN EPISODIC LUTEINIZING-HORMONE RELEASE IN OVARIECTOMIZED RATS - AN EXCITATORY COMPONENT AND OPIOID INVOLVEMENT, Endocrinology, 133(2), 1993, pp. 747-754
Citations number
51
Categorie Soggetti
Endocrynology & Metabolism
Journal title
ISSN journal
00137227
Volume
133
Issue
2
Year of publication
1993
Pages
747 - 754
Database
ISI
SICI code
0013-7227(1993)133:2<747:RONIEL>2.0.ZU;2-M
Abstract
We tested the hypothesis that hypothalamic neuropeptide-Y (NPY) is an excitatory signal in the episodic secretion of LH in ovariectomized (o vx) rats and that the suppression of LH secretion that consistently fo llows intracerebroventricular administration of NPY is due to concurre nt release of opioids or CRH, both previously shown to readily inhibit LH release. In the first experiment, ovx rats received continuous int raventricular infusion of either serum containing NPY antibodies (NPY- Ab) or normal rabbit serum (control) at dilutions of 1:5 or 1:1. NPY-A b infusion at a 1:5 dilution significantly decreased mean plasma LH le vels and LH pulse amplitude without affecting LH pulse frequency over a 3-h period of observation. However, infusion of relatively more conc entrated NPY-Ab (1:1) markedly decreased not only mean plasma LH level s and LH pulse amplitude, but also the frequency of LH episodes. In th e next experiment, we observed that intraventricular administration of NPY (0.2 nmol) suppressed LH release for 60 min. However, blockade of opiate receptors with iv infusion of naloxone (2 mg/h) before and aft er NPY injection completely counteracted the NPY-induced inhibition of LH release. On the other hand, prior blockade of the CRH receptors wi th alpha-helical CRH-(9-41) (25 or 100 mug/rat) was ineffective in rev ersing the inhibitory LH response of NPY (0.125 nmol). These results t ogether with our previous demonstration of morphological communication between NPY and beta-endorphin neurons, show that suppression of LH b y exogenous NPY in ovx rats may result from concurrent stimulation of opioids, primarily beta-endorphin. However, diminution of all paramete rs of episodic LH secretion by NPY-Ab affirms the notion that the NPY network is a physiologically important excitatory component of the hyp othalamic pulse generator circuitry that regulates episodic LH secreti on in rats.