Restricted role of CRF1 receptor for the activity of brainstem catecholaminergic neurons in the negative state of morphine withdrawal

García-Carmona, Juan Antonio; Almela, Pilar; Baroja‐Mazo, Alberto; Milanés, M. Victoria; Laorden, María‐Luisa

doi:10.1007/s00213-011-2478-y

Cited by 19 publications

(18 citation statements)

References 46 publications

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“…Our results are consistent with findings from our laboratory demonstrating that CRF1 receptor is not implicated in the enhancement of NA turnover in the PVN, which receives projections from NTS, observed during morphine withdrawal [33]. In addition, a previous study using CRF1receptor-deficient mice demonstrated that CRF1 receptor is not responsible for the phosphorylation of TH observed in NTS after naloxone-precipitated withdrawal in wild-type mice [56].…”

Section: Discussionsupporting

confidence: 93%

“…Together, all these data implicated NA neurons in NTS in the aversiveness of acute opioid withdrawal. Support for this idea can be found in a number of studies that implicate the NTS-A2 noradrenergic cells group in that affective disorder associated with drug withdrawal [6], [54]–[56]. Changes in the state of phosphorylation of TH, the rate limiting enzyme in the synthesis of catecholamines, are critically involved in the regulation of catecholamines, synthesis and function.…”

Section: Discussionmentioning

confidence: 94%

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Role of Corticotropin-Releasing Factor (CRF) Receptor-1 on the Catecholaminergic Response to Morphine Withdrawal in the Nucleus Accumbens (NAc)

et al. 2012

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Stress induces the release of the peptide corticotropin-releasing factor (CRF) into the ventral tegmental area (VTA), and also increases dopamine (DA) levels in brain regions receiving dense VTA input. Since the role of stress in drug addiction is well established, the present study examined the possible involvement of CRF1 receptor in the interaction between morphine withdrawal and catecholaminergic pathways in the reward system. The effects of naloxone-precipitated morphine withdrawal on signs of withdrawal, hypothalamo-pituitary-adrenocortical (HPA) axis activity, dopamine (DA) and noradrenaline (NA) turnover in the nucleus accumbens (NAc) and activation of VTA dopaminergic neurons, were investigated in rats pretreated with vehicle or CP-154,526 (selective CRF1R antagonist). CP-154,526 attenuated the increases in body weight loss and suppressed some of withdrawal signs. Pretreatment with CRF1 receptor antagonist resulted in no significant modification of the increased NA turnover at NAc or plasma corticosterone levels that were seen during morphine withdrawal. However, blockade of CRF1 receptor significantly reduced morphine withdrawal-induced increases in plasma adrenocorticotropin (ACTH) levels, DA turnover and TH phosphorylation at Ser40 in the NAc. In addition, CP-154,526 reduced the number of TH containing neurons expressing c-Fos in the VTA after naloxone-precipitated morphine withdrawal. Altogether, these results support the idea that VTA dopaminergic neurons are activated in response to naloxone-precipitated morphine withdrawal and suggest that CRF1 receptors are involved in the activation of dopaminergic pathways which project to NAc.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 94%

Role of Corticotropin-Releasing Factor (CRF) Receptor-1 on the Catecholaminergic Response to Morphine Withdrawal in the Nucleus Accumbens (NAc)

et al. 2012

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“…Some studies have reported that immobility and climbing behavior in the FST are associated with the central noradrenergic system [21]. Also, many studies have suggested that morphine dependence and withdrawal show increases the number of TH positive neurons in the LC [22,23]. Activation of the LC produces intense anxiety, hypervigilance and inhibition of exploratory behavior [24,25].…”

Section: Discussionmentioning

confidence: 99%

Effect of Berberine on Depression- and Anxiety-Like Behaviors and Activation of the Noradrenergic System Induced by Development of Morphine Dependence in Rats

Lee

Sur

Yeom

et al. 2012

Korean J Physiol Pharmacol

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The purpose of this study was to evaluate whether berberine (BER) administration could attenuate depression-and anxiety-like behaviors and increase corticotrophin-releasing factor (CRF) and tyrosine hydroxylase (TH) expression following chronic morphine withdrawal in rats. Male rats were exposed to chronic, intermittent, escalating morphine (10∼ 50 mg/kg) for 10 days. After the last morphine injection, depression-and anxiety-like beahvior associated with morphine discontinuation persisted for at least three days during withdrawal without any change in ambulatory activity. Daily BER administration significantly decreased immobility in the forced swimming test and increased open-arm exploration in the elevated plus maze test. BER administration also significantly blocked the increase in hypothalamic CRF expression and TH expression in the locus coeruleus (LC) and the decrease in hippocampal brain-derived neurotrophic factor (BDNF) mRNA expression. Taken together, these findings demonstrated that BER administration significantly reduced morphine withdrawal-associated behaviors following discontinuation of repeated morphine administration in rats, possibly through modulation of hypothalamic CRF and the central noradrenergic system. BER may be a useful agent for treating or alleviating complex withdrawal symptoms and preventing morphine use relapses.

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“…A CRF 1 antagonist also prevented the development of a conditioned place aversion following precipitated withdrawal in opioid-dependent rats (Stinus, Cador, Zorrilla, & Koob, 2005). Similarly, Crhr1 knockout mice did not show opioid withdrawal-induced conditioned place aversion (Contarino & Papaleo, 2005; Garcia-Carmona, Almela, Baroja-Mazo, Milanes, & Laorden, 2012). Finally, systemic injections of brain-penetrant CRF 1 antagonists reduced the heightened anxiety-like behavior of dependent rodents acutely withdrawn from alcohol or other substances of abuse (Breese, Overstreet, & Knapp, 2005; Breese, Overstreet, Knapp, & Navarro, 2005; Gehlert et al, 2007; Knapp et al, 2004; Overstreet et al, 2004; Sommer et al, 2008).…”

Section: Role For Crf-crf1 Systems In Animal Models Of Addictionmentioning

confidence: 97%

Corticotropin-Releasing Factor (CRF) and Addictive Behaviors

Roberto

Spierling

Kirson

et al. 2017

International Review of Neurobiology

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Drug addiction is a complex disorder that is characterized by compulsivity to seek and take the drug, loss of control in limiting intake of the drug, and emergence of a withdrawal syndrome in the absence of the drug. The transition from casual drug use to dependence is mediated by changes in reward and brain stress functions and has been linked to a shift from positive reinforcement to negative reinforcement. The recruitment of brain stress systems mediates the negative emotional state produced by dependence that drives drug seeking through negative reinforcement mechanisms, defined as the “dark side” of addiction. In this chapter we focus on behavioral and cellular neuropharmacological studies that have implicated brain stress systems (i.e., corticotropin-releasing factor [CRF]) in the transition to addiction and the predominant brain regions involved. We also discuss the implication of CRF recruitment in compulsive eating disorders.

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Restricted role of CRF1 receptor for the activity of brainstem catecholaminergic neurons in the negative state of morphine withdrawal

Cited by 19 publications

References 46 publications

Role of Corticotropin-Releasing Factor (CRF) Receptor-1 on the Catecholaminergic Response to Morphine Withdrawal in the Nucleus Accumbens (NAc)

Role of Corticotropin-Releasing Factor (CRF) Receptor-1 on the Catecholaminergic Response to Morphine Withdrawal in the Nucleus Accumbens (NAc)

Effect of Berberine on Depression- and Anxiety-Like Behaviors and Activation of the Noradrenergic System Induced by Development of Morphine Dependence in Rats

Corticotropin-Releasing Factor (CRF) and Addictive Behaviors

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