Endogenous opioid peptides and hypothalamic neuroendocrine neurones

Abstract

This consideration of the influence of endogenous opioid peptide systems on GnRH and oxytocin neurones serves to illustrate some of their possible regulatory interactions with other neuroendocrine systems. Opioids are known to influence the secretion of all the anterior pituitary hormones (see Grossman & Rees, 1983) and these effects are likely to be mediated, at least in part, in the hypothalamus. For example, inhibitory effects of opioids have also been described on secretion from the median eminence of somatostatin (Drouva et al. 1981b) and dopamine (Wilkes & Yen, 1980), and this site of action probably accounts for at least some of the stimulatory effects of exogenous opioids on plasma growth hormone and prolactin levels respectively. For the GnRH neurones the influence of endogenous opioid neurones, possibly the arcuate beta-endorphin system, appears to be mediated indirectly by inhibiting release of excitatory or facilitatory monoamines. This opioid-adrenergic interaction itself appears to be central in the regulation of gonadotrophin secretion and mediation of the feedback effects of gonadal steroids in the brain. The steroids may act directly on both adrenergic and opioid neurones, altering monoamine metabolism and release which may, in turn, regulate numbers of adrenergic receptors perhaps located on the GnRH neurones. Opioid peptide levels are also modulated by steroids probably reflecting altered synthesis and/or processing of precursors. Regulation of the opioid-adrenergic input may not only acutely affect the secretory output of the GnRH neurones but also influence synthesis or processing of GnRH itself (see Kalra & Kalra, 1984) and its degradation by hypothalamic peptidases (Advis, Krause & McKelvy, 1983). Oxytocin neurones demonstrate three further levels of interaction with endogenous opioid peptides. First the anatomical organization of the oxytocin neurones has enabled a clear demonstration of the action of opioids close to the secretory terminals to uncouple the generation of electrical activity from release of peptide. Secondly, both the oxytocin and the neighbouring vasopressin neurones themselves synthesize, process and package opioid peptides. These neurones thus provide a clear example of co-existence of several biologically active products in individual neurones. The relative expression of the different gene products may prove to be a further level of control of opioid influences on the oxytocin and vasopressin neurones.(ABSTRACT TRUNCATED AT 400 WORDS)

Naloxone decreases the inhibitory effect of alprazolam on the release of adrenocorticotropin/cortisol induced by physical exercise in man

“…Our experimental conditions cannot clarify the site of action of the opiate/GABA/BZD interactions in the inhibition of exercise-stimulated ACTH secretion. The effect of ALP might be exerted at the pituitary level, where opioids are known to reduce ACTH secretion or in the hypothalamus where endogenous opioids are thought to inhibit corticotrophin releasing hormone (CRH) release [7,14,15].…”

Effects of naloxone or transient weaning on secretion of LH and prolactin in lactating sows

“…Studies utilizing opiate agonists and antagonists have demonstrated that endogenous opioid peptides inhibit LH and stimulate prolactin (Meites et al, 1979;Grossman & Rees, 1983;Bicknell, 1985;Malven, 1986). Administration of naloxone, an opioid antagonist, during lactation resulted in increased LH in rats (Sirinathsinghji & Martini, 1984), ewes (Gregg et al, 1986), cows , women (Ishizuka et al, 1984) and sows Mattioli et al, 1986) and suppressed serum prolactin in rats (Ferland et al, 1978;Miki et al, 1981;Sirinathsinghji & Martini, 1984), ewes (Gregg et al, 1986) and sows (Mattioli et al, 1986).…”

Estrogen-Induced Alteration of μ-Opioid Receptor Immunoreactivity in the Medial Preoptic Nucleus and Medial Amygdala

“…Several lines of evidence implicate endogenous opioid peptides in the regulation of puberty (Wilkinson and Bhanot, 1982;Bhanot and Wilkinson, 1983;Sirinathsinghji et al, 1985;Rodriguez et al, 1993), secretion of luteinizing hormone (Cicero et al, 1979;Kalra and Kalra, 1984;Piva et al, 1985;Zhen and Gallo, 1992) through alterations of luteinizing hormone-releasing hormone (LHRH) release (Bicknell, 1985;Kalra, 1986;Piva et al, 1986;Jacobson and Kalra, 1989), and female sexual behavior (Wiesner and Moss, 1986a,b;Pfaus and Gorzalka, 1987;Vathy et al, 1991;Pfaus and Pfaff, 1992;Allen et al, 1993;Olster, 1994;Torii et al, 1995Torii et al, , 1996Sinchak et al, 1997a). Endogenous opioid peptides also modulate the estrogeninduced expression and release of other transmitters that alter reproductive behavior, such as cholecystokinin and substance P (Eckersell and Micevych, 1997;Sinchak et al, 1997b), norepinephrine (Vathy et al, 1991), and serotonin (Allen et al, 1993).…”