Effects of morphine and morphine withdrawal on brainstem neurons innervating hypothalamic nuclei that control thepituitary‐adrenocortical axis in rats

Laorden, M. Luisa; Castells, María Teresa; Milanés, M. Victoria

doi:10.1038/sj.bjp.0704684

Cited by 51 publications

(74 citation statements)

References 39 publications

(59 reference statements)

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“…PrRP is highly expressed in A1 and A2 noradrenergic neurons of the caudal medulla, which are activated by pain signals and opioid withdrawal 36,37 . These noradrenergic neurons are well known to be anatomically connected with other brain areas involved in nociceptive and emotional pathways, which might explain the large array of effects observed.…”

Section: Discussionmentioning

confidence: 99%

The prolactin-releasing peptide antagonizes the opioid system through its receptor GPR10

et al. 2005

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Prolactin-releasing peptide (PrRP) and its receptor G protein-coupled receptor 10 (GPR10) are expressed in brain areas involved in the processing of nociceptive signals. We investigated the role of this new neuropeptidergic system in GPR10-knockout mice. These mice had higher nociceptive thresholds and stronger stress-induced analgesia than wild-type mice, differences that were suppressed by naloxone treatment. In addition, potentiation of morphine-induced antinociception and reduction of morphine tolerance were observed in mutants. Intracerebroventricular administration of PrRP in wild-type mice promoted hyperalgesia and reversed morphine-induced antinociception. PrRP administration had no effect on GPR10-mutant mice, showing that its effects are mediated by GPR10. Anti-opioid effects of neuropeptide FF were found to require a functional PrRP-GPR10 system. Finally, GPR10 deficiency enhanced the acquisition of morphine-induced conditioned place preference and decreased the severity of naloxone-precipitated morphine withdrawal syndrome. Altogether, our data identify the PrRP-GPR10 system as a new and potent negative modulator of the opioid system.Opiate drugs, the prototype of which is morphine, are used largely for the treatment of severe pain. However, the prolonged use of opiate drugs induces a behavioral adaptation that results in the development of tolerance and dependence 1 . Although these adaptive mechanisms have been known for decades, the underlying pathophysiological pathways have not been fully clarified. It has been proposed that the opioid receptor signaling pathway is adaptively regulated at the cellular level, although more recently a growing contribution of the plasticity of neuronal networks involving opioidergic neurons has been recognized. In support of this latter hypothesis, a number of neuropeptides, including cholecystokinin (CCK) 2 , neuropeptide FF (NPFF) 3 and nociceptin (orphanin FQ) 4 , have been proposed as modulators of the opioid system. These various peptidergic pathways are collectively designated as an anti-opioid system. However, the action of individual peptides on the opioid pathway and on the processing of nociceptive signals is complex and some aspects remain controversial, particularly as the behavioral consequences can vary depending on the injection site of these peptides and the precise experimental setup 5,6 . Among these peptides, NPFF, which belongs to the RF-amide peptide family, was shown (among other actions) to regulate blood pressure 7 , prolactin release 8 and nociceptive signal processing 9 . Prolactin-releasing peptide (PrRP) has recently been identified as an additional member of the mammalian RF-amide peptide family, following its isolation as the natural agonist of the previously orphan GPR10 (ref. 10) (also known as hGR3 in human or UHR-1 in rat). Intracerebroventricular (i.c.v.) administration of PrRP affects feeding behavior 11 , blood pressure 12 and neuroendocrine processes, such as corticotropin-releasing hormone (CRH) 13 and oxytocin 14 release.In a...

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Section: Discussionmentioning

confidence: 99%

The prolactin-releasing peptide antagonizes the opioid system through its receptor GPR10

et al. 2005

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“…Activation of afferents from gastrointestinal, cardiovascular, and respiratory targets supported widespread stimulation of CA NTS neurons in various behaviors including sleep and stress (Murphy et al, 1994;Chan and Sawchenko, 1998;Dayas et al, 2004;Kubin et al, 2006). Furthermore, changes in blood pressure (Chan and Sawchenko, 1998), opioid withdrawal (Laorden et al, 2002), noxious stimuli (Jin et al, 1994), and immune challenge (Lacroix and Rivest, 1997) activate c-fos expression in subpopulations of NTS CA neurons. Thus, visceral afferent regulation of the NTS CA neurons is broadly implicated in homeostatic control and the NTS CA cell groups likely provide the critical link with other brain regions that produce the behavioral outcomes.…”

Section: Visceral Integration and Nts Ca Neuronsmentioning

confidence: 99%

Visceral Afferents Directly Activate Catecholamine Neurons in the Solitary Tract Nucleus

et al. 2007

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“…All abused drugs, including ethanol (EtOH), have effects that mirror stressors in their activation of the hypothalamic-pituitary-adrenal (HPA) axis, via central mechanisms (17)(18)(19)(20) that depend on the stimulation of CRF-containing neurons of the paraventricular nucleus of the hypothalamus. CRF is a primary activator of the HPA axis and an essential mediator of behavioral and autonomic outcomes of stress.…”

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confidence: 99%

Corticotropin-releasing factor-1 receptor involvement in behavioral neuroadaptation to ethanol: A urocortin ₁ -independent mechanism

Pastor

McKinnon

Scibelli

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

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A common expression of neuroadaptations induced by repeated exposure to addictive drugs is a persistent sensitized behavioral response to their stimulant properties. Neuroplasticity underlying drug-induced sensitization has been proposed to explain compulsive drug pursuit and consumption characteristic of addiction. The hypothalamic-pituitary-adrenal (HPA) axis-activating neuropeptide, corticotropin-releasing factor (CRF), may be the keystone in drug-induced neuroadaptation. Corticosterone-activated glucocorticoid receptors (GRs) mediate the development of sensitization to ethanol (EtOH), implicating the HPA axis in this process. EtOHinduced increases in corticosterone require CRF activation of CRF1 receptors. We posited that CRF1 signaling pathways are crucial for EtOH-induced sensitization. We demonstrate that mice lacking CRF1 receptors do not show psychomotor sensitization to EtOH, a phenomenon that was also absent in CRF 1 ؉ 2 receptor doubleknockout mice. Deletion of CRF2 receptors alone did not prevent sensitization. A blunted endocrine response to EtOH was found only in the genotypes showing no sensitization. The CRF1 receptor antagonist CP-154,526 attenuated the acquisition and prevented the expression of EtOH-induced psychomotor sensitization. Because CRF1 receptors are also activated by urocortin-1 (Ucn1), we tested Ucn1 knockout mice for EtOH sensitization and found normal sensitization in this genotype. Finally, we show that the GR antagonist mifepristone does not block the expression of EtOH sensitization. CRF and CRF1 receptors, therefore, are involved in the neurobiological adaptations that underlie the development and expression of psychomotor sensitization to EtOH. A CRF/CRF1-mediated mechanism involving the HPA axis is proposed for acquisition, whereas an extrahypothalamic CRF/CRF1 participation is suggested for expression of sensitization to EtOH.addiction ͉ CP-154,526 ͉ HPA axis ͉ knockout mice ͉ psychomotor sensitization

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Effects of morphine and morphine withdrawal on brainstem neurons innervating hypothalamic nuclei that control thepituitary‐adrenocortical axis in rats

Cited by 51 publications

References 39 publications

The prolactin-releasing peptide antagonizes the opioid system through its receptor GPR10

The prolactin-releasing peptide antagonizes the opioid system through its receptor GPR10

Visceral Afferents Directly Activate Catecholamine Neurons in the Solitary Tract Nucleus

Corticotropin-releasing factor-1 receptor involvement in behavioral neuroadaptation to ethanol: A urocortin ₁ -independent mechanism

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Effects of morphine and morphine withdrawal on brainstem neurons innervating hypothalamic nuclei that control thepituitary‐adrenocortical axis in rats

Cited by 51 publications

References 39 publications

The prolactin-releasing peptide antagonizes the opioid system through its receptor GPR10

The prolactin-releasing peptide antagonizes the opioid system through its receptor GPR10

Visceral Afferents Directly Activate Catecholamine Neurons in the Solitary Tract Nucleus

Corticotropin-releasing factor-1 receptor involvement in behavioral neuroadaptation to ethanol: A urocortin 1 -independent mechanism

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Corticotropin-releasing factor-1 receptor involvement in behavioral neuroadaptation to ethanol: A urocortin ₁ -independent mechanism