Contribution of the Supra-Optic Nucleus to Brain and Pituitary Pools of Immunoreactive Vasopressin and Particular Opioid Peptides, and the Interrelationships between These, in the Rat

Millan, Mark J.; Millan, M.H.; Herz, A.

doi:10.1159/000123473

Cited by 34 publications

(5 citation statements)

References 36 publications

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“…Watson et al (1982) have shown that immunoreactivity associated with dynorphin was colocalized with AVP in the hypothalamo-hypophyseal tract. In addition lesions of the supraoptic nucleus produce a parallel decrease in ir-AVP and ir-Dyn A in the NIL (Millan et al, 1983). The results of the present study d o not rule out the existence of a subpopulation of neurons in the magnocellular group in hypothalamus in which colocalization of dynorphinlike opioid peptides with AVP occurs.…”

Section: Discussioncontrasting

confidence: 88%

Subcellular Distribution of Opioid Peptides in Rat Hypothalamus and Pituitary

Molineaux

Rosenberger

Cox

1984

Journal of Neurochemistry

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Homogenates of rat anterior lobe (AL) and neurointermediate lobe (NIL) pituitary and rat hypothalamus were subjected to subcellular fractionation and density gradient centrifugation. The subcellular distribution of immunoreactive dynorophin A (ir-Dyn A) in NIL was found to be similar to that of ir-arginine vasopressin (ir-AVP). ir-Dyn A migrated as a discrete band on sucrose density gradients, which corresponded in sedimentation rate to that of ir-AVP, suggesting that these two peptides are stored within organelles of similar size and density. Two other products of prodynorphin, ir-alpha-neoendorphin (ir-alpha-nEND) and ir-Dyn A-(1-8) also comigrated with ir-AVP. ir-[Leu5]-enkephalin (ir-LE), which may be a product of prodynorphin or proenkephalin, was also found to migrate in this region of the gradient. When a homogenate of rat hypothalamus was prepared using a method that has been developed for synaptosome isolation, ir-Dyn A was found to comigrate with Na+/K+-activated adenosine triphosphatase (Na/K-ATPase), a synaptosomal marker enzyme. Using a more concentrated homogenate ir-Dyn A was found to migrate to a less dense region where peptide-containing synaptic vesicles have previously been localized. When a synaptosomal preparation was lysed in hypotonic solution a shift was seen in the migration rate of ir-Dyn A to this region of the gradient (containing putative synaptic vesicles). Thus the bulk of hypothalamic dynorphin appears to be present within synaptosome-like structures which, upon lysis, release a less dense, smaller subcellular organelle corresponding in sedimentation characteristics to other types of peptide-containing synaptic vesicles.(ABSTRACT TRUNCATED AT 250 WORDS)

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Section: Discussioncontrasting

confidence: 88%

Subcellular Distribution of Opioid Peptides in Rat Hypothalamus and Pituitary

Molineaux

Rosenberger

Cox

1984

Journal of Neurochemistry

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“…Thus the oxytocin and vasopressin neurones synthesize and process proenkephalin and prodynorphin respectively. However, on a molar basis the concentrations of opioid peptides in the rat neuro¬ hypophysis are at least a thousand-fold lower than those of oxytocin and vasopressin (Millan, Millan & Herz, 1983). There is thus considerable differentiation in the expression of the oxytocin/vasopressin and proenkephalin/pro-dynorphin genes.…”

Section: Opioids Monoamines and Gnrh Neuronesmentioning

confidence: 96%

Endogenous opioid peptides and hypothalamic neuroendocrine neurones

Bicknell¹

1985

Journal of Endocrinology

153

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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)

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“…We conclude that endogenous opioid peptides inhibit release of oxytocin in vivo by an effect on the final common pathway, i.e. the magnocellular neuron or on pituicytes in the neural lobe.A growing body of evidence supports a role for endoge nous opioid peptides in attenuating release of vasopressin and oxytocin from the hypothalamo-neurohypophysial sys tem [ 16,32] during osmotic and nonosmotic stimulation (22,27], Opioid peptides are localized both within magnocellu lar neurons that synthesize either vasopressin or oxytocin (13,35,36] and in the surrounding hypothalamus [15,17,18,25], In addition, opiate receptors are present in the neural lobe of the pituitary [28,34] and in the supraoptic and par aventricular nuclei of the hypothalamus [34]. Thus, both the cell bodies and nerve terminals of magnocellular neurons are sites where opioid peptides could attenuate secretion of neurohypophysial hormones.…”

mentioning

confidence: 99%

Naloxone Effects on Plasma Vasopressin and Oxytocin Concentrations Elevated by Histamine, Nicotine, Isoproterenol and an Acute Increase in [NaCl] in Cerebrospinal Fluid

Summy-Long¹,

Denlinger²,

Palm³

et al. 1986

Neuroendocrinology

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Endogenous opioid peptides inhibit secretion of oxytocin during dehydration, hemorrhage and parturition and attenuate release of vasopressin by tail electroshock. Diverse agents were used to stimulate the hypothalamo-neurohypophysial system to investigate the hypothesis that if oxytocin (or vasopressin) release were inhibited by opioid peptides regardless of the stimulus, the site of opiate action may be in the final common pathway (i.e. the magnocellular neuron) or on pituicytes in the neural lobe. Using male Sprague-Dawley rats, we therefore investigated the effect of an opiate receptor antagonist, naloxone (5 mg/kg s.c), on the plasma concentrations of oxytocin and vasopressin elevated by various pharmacologic stimuli, including histamine (10 mg/kg i.p.), nicotine (0.15 or 1.5 mg/kg i.p.), isoproterenol (30 or 120 ug/kg i.m.) and increased [NaCl] in cerebrospinal fluid (CSF; 10 µl artificial CSF containing 1 MNaCl i.v.t.). Control animals received saline (0.85%) or artificial CSF (containing 0.16 M NaCl). Animals were decapitated 60 s (†[NaCΓJ in CSF) or 10 min after the stimulus or vehicle. Vasopressin and oxytocin were extracted from plasma and quantified by RIA. The concentrations of oxytocin and vasopressin in plasma were elevated (p < 0.05) by histamine, isoproterenol (30 and 120 αg/ kg), ↑[NaCl] in CSF, and nicotine at the higher (1.5 mg/kg) but not lower (0.15 mg/kg) dose. Naloxone increased further (p<0.05) the concentration of oxytocin in plasma after histamine, nicotine (0.15 and 1.5 mg/kg), isoproterenol (30 and 120 µg/kg) and ↑[NaCl] in CSF. Naloxone also increased (p<0.05) oxytocin concentration in controls receiving CSF or saline. Vasopressin concentration was unaffected by naloxone in either controls or after any of the stimuli. We conclude that endogenous opioid peptides inhibit release of oxytocin in vivo by an effect on the final common pathway, i.e. the magnocellular neuron or on pituicytes in the neural lobe.

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Contribution of the Supra-Optic Nucleus to Brain and Pituitary Pools of Immunoreactive Vasopressin and Particular Opioid Peptides, and the Interrelationships between These, in the Rat

Cited by 34 publications

References 36 publications

Subcellular Distribution of Opioid Peptides in Rat Hypothalamus and Pituitary

Subcellular Distribution of Opioid Peptides in Rat Hypothalamus and Pituitary

Endogenous opioid peptides and hypothalamic neuroendocrine neurones

Naloxone Effects on Plasma Vasopressin and Oxytocin Concentrations Elevated by Histamine, Nicotine, Isoproterenol and an Acute Increase in [NaCl] in Cerebrospinal Fluid

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