Endocrinology, Vol 104, 1286-1291, Copyright © 1979 by Endocrine Society

ARTICLES

Endogenous opioids participate in the regulation of the hypothalamus- pituitary-luteinizing hormone axis and testosterone's negative feedback control of luteinizing hormone

TJ Cicero, BA Schainker and ER Meyer

Two narcotic antagonists, naloxone and naltrexone, significantly elevated serum LH levels in male rats within minutes after their sc injection. The peak increase in serum LH occurred 20 min after the injection. Naloxone increased LH levels up to a dose of 1 mg/kg, after which no further increases were found. A dose of 0.35 mg/kg produced a half-maximal response. The exogenous opioid morphine blocked the increase in LH produced by naloxone in a dose-dependent fashion, suggesting that the specific receptor-blocking effects of the antagonist could account for its enhancement of serum LH levels. The locus of action of naloxone within the hypothalamic-pituitary-LH axis appeared to be at the level of the hypothalamus since the drug had no effect on LHRH-stimulated release of LH by the anterior pituitary and did not block dihydrotestosterone's suppression of pituitary LH release in vitro. Naloxone also prevented testosterone's negative feedback inhibition of serum LH in the castrated male rat. The results of these studies suggest that endogenous opioids exist in brain tissue which normally inhibit activity in the hypothalamic-pituitary-LH axis and participate in the androgen-dependent feedback control of LH elaboration by this axis.

This article has been cited by other articles:

				B. Dudas and I. Merchenthaler Topography and Associations of Leu-Enkephalin and Luteinizing Hormone-Releasing Hormone Neuronal Systems in the Human Diencephalon J. Clin. Endocrinol. Metab., April 1, 2003; 88(4): 1842 - 1848. [Abstract] [Full Text] [PDF]

				X Wu, A S Faqi, J Yang, X Ding, X Jiang, and I Chahoud Male reproductive toxicity and b-luteinizing hormone gene expression in sexually mature and immature rats exposed to 2-bromopropane Human and Experimental Toxicology, November 1, 1999; 18(11): 683 - 690. [Abstract] [PDF]

				A. P. Cemeroglu, G. B. Kletter, W. Guo, M. B. Brown, R. P. Kelch, J. C. Marshall, V. Padmanabhan, and C. M. Foster In Pubertal Girls, Naloxone Fails to Reverse the Suppression of Luteinizing Hormone Secretion by Estradiol J. Clin. Endocrinol. Metab., October 1, 1998; 83(10): 3501 - 3506. [Abstract] [Full Text]

				M.-F. Cheng, J. P. Peng, and P. Johnson Hypothalamic Neurons Preferentially Respond to Female Nest Coo Stimulation: Demonstration of Direct Acoustic Stimulation of Luteinizing Hormone Release J. Neurosci., July 15, 1998; 18(14): 5477 - 5489. [Abstract] [Full Text] [PDF]

				C. B. Eckersell, P. Popper, and P. E Micevych Estrogen-Induced Alteration of µ-Opioid Receptor Immunoreactivity in the Medial Preoptic Nucleus and Medial Amygdala J. Neurosci., May 15, 1998; 18(10): 3967 - 3976. [Abstract] [Full Text] [PDF]

				S. Pu, T. L. Horvath, S. Diano, F. Naftolin, P. S. Kalra, and S. P. Kalra Evidence Showing That {beta}-Endorphin Regulates Cyclic Guanosine 3',5'-Monophosphate (cGMP) Efflux: Anatomical and Functional Support for an Interaction between Opiates and Nitric Oxide Endocrinology, April 1, 1997; 138(4): 1537 - 1543. [Abstract] [Full Text] [PDF]