Social conflict-induced changes in nociception and β-endorphin-like immunoreactivity in pituitary and discrete brain areas of C57BL/6 and DBA/2 mice

Külling, P.; Frischknect, Hans-Rudolf; Pasi, Aurelio; Waser, Peter G.; Siegfried, Bert

doi:10.1016/0006-8993(88)91563-6

Cited by 41 publications

(10 citation statements)

References 49 publications

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“…Given the preliminary findings that repeated social stress produces a decrease in LC discharge rate that is apparent 2 days after the last stress, we expect that this is due to the engagement of ENK afferents to the LC and so ppENK is predicted to be upregulated in LC afferents of social stressed rats at this time. This would be consistent with studies showing heightened analgesia following social defeat (Miczek, 1991; Rodgers & Randall, 1985) which is thought to reflect an increase in endogenous opioid release in brain regions associated with pain processes (Kulling, Frischknecht, Pasi, Waser, & Siegfried, 1988). Interestingly, ENK is co-localized with Glu in LC afferents (Barr & Van Bockstaele, 2005; E.…”

Section: Stress-induced Molecular and Cellular Plasticity That Sesupporting

confidence: 90%

Neuropeptide Regulation of the Locus Coeruleus and Opiate-Induced Plasticity of Stress Responses

Bockstaele

Valentino

2013

A New Era of Catecholamines in the Laboratory and Clinic

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Stress has been implicated as a risk factor in vulnerability to the initiation and maintenance of opiate abuse and is thought to play an important role in relapse in subjects with a history of abuse. Conversely, chronic opiate use and withdrawal are stressors and can potentially predispose individuals to stress-related psychiatric disorders. Because the interaction of opiates with stress response systems has potentially widespread clinical consequences, it is important to delineate how specific substrates of the stress response and endogenous opioid systems interact and the specific points at which stress circuits and endogenous opioid systems intersect. The purpose of this review is to present and discuss the results of studies that have unveiled the complex circuitry by which stress-related neuropeptides and endogenous opioids co-regulate activity of the locus coeruleus (LC)-norepinephrine (NE) system and how chronic morphine, or stress, disturbs this regulation.

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Section: Stress-induced Molecular and Cellular Plasticity That Sesupporting

confidence: 90%

Neuropeptide Regulation of the Locus Coeruleus and Opiate-Induced Plasticity of Stress Responses

Bockstaele

Valentino

2013

A New Era of Catecholamines in the Laboratory and Clinic

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“…When an intruder mouse is attacked frequently and eventually displays the characteristic defeat response pattern (upright posture, retracted fore limbs, vocalizations), it develops an opioid-like analgesia. This analgesia is blocked by centrally acting mu-opioid receptor antagonists, and is concurrent with elevated beta-endorphin and met-enkephalin levels in several brain regions (Siegfried et al, 1984; Teskey et al, 1984; Rodgers & Randall, 1985; Miczek et al, 1986; Külling et al, 1988; Miczek et al, 1991). Similarly, acutely defeated rats show a potentiated analgesic response to mu and delta opioid receptor agonists ([ d -Ala 2 , N -Me-Phe 4 Gly 5 -ol]-enkephalin (DAMGO) and [ d -Pen 2 , d -Pen 5 ]-enkephalin (DPDPE), respectively), and this potentiation is reversed by the receptor-selective antagonists, involving receptor sites in the periaqueductal grey area (Vivian & Miczek, 1998; Vivian & Miczek, 1999).…”

Section: Neurobiological Characteristics Therapeutics and Drug Abusementioning

confidence: 99%

Social stress, therapeutics and drug abuse: Preclinical models of escalated and depressed intake

Miczek

Yap

Covington

2008

Pharmacology & Therapeutics

295

252

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The impact of ostensibly aversive social stresses on triggering, amplifying and prolonging intensely rewarding drug taking is an apparent contradiction in need of resolution. Social stress encompasses various types of significant life events ranging from maternal separation stress, brief episodes of social confrontations in adolescence and adulthood, to continuous subordination stress, each with its own behavioral and physiological profile. The neural circuit comprising the VTA–accumbens–PFC–amygdala is activated by brief episodes of social stress, which is critical for the DA-mediated behavioral sensitization and increased stimulant consumption. A second neural circuit comprising the raphe–PFC–hippocampus is activated by continuous subordination stress and other types of uncontrollable stress. In terms of the development of therapeutics, brief maternal separation stress has proven useful in characterizing compounds acting on subtypes of GABA, glutamate, serotonin and opioid receptors with anxiolytic potential. While large increases in alcohol and cocaine intake during adulthood have been seen after prolonged maternal separation experiences during the first two weeks of rodent life, these effects may be modulated by additional yet to be identified factors. Brief episodes of defeat stress can engender behavioral sensitization that is relevant to escalated and prolonged self-administration of stimulants and possibly opioids, whereas continuous subordination stress leads to anhedonia-like effects. Understanding the intracellular cascade of events for the transition from episodic to continuous social stress in infancy and adulthood may provide insight into the modulation of basic reward processes that are critical for addictive and affective disorders.

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“…Initial pharmacological data implicated endogenous opioid peptides and their receptors in the mediation of the antinociceptive response in mice experiencing social defeat stress. Opioid receptor antagonists such as naloxone, naltrexone and β -chlornaltrexamine blocked the defeat stress-induced analgesia (Frischknecht and Siegfried 1989; Külling et al 1988; Miczek et al 1982, 1985; Rodgers and Randall 1985; Siegfried and Frischknecht 1989; Teskey et al 1984). The quaternary forms of naloxone and naltrexone that do not readily penetrate the blood brain barrier failed to antagonize the defeat stress-induced analgesia, pointing to a site of action in the central nervous system (Miczek et al 1982; Rodgers and Randall 1985).…”

Section: Introductionmentioning

confidence: 99%

“…The role of the μ opioid receptors in the action of this effect of defeat stress is further shown by the selective antagonism by naltrexone, but not by naltrindole, of stress-potentiated DAMGO analgesia (Vivian and Miczek 1998). After more frequent attacks, β -endorphin-like immunoreactivity decreased in the periaqueductal region of intruder mice (Külling et al 1988). …”

Section: Introductionmentioning

confidence: 99%

Gene Expression in Aminergic and Peptidergic Cells During Aggression and Defeat: Relevance to Violence, Depression and Drug Abuse

et al. 2011

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In this review, we examine how experiences in social confrontations alter gene expression in mesocorticolimbic cells. The focus is on the target of attack and threat due to the prominent role of social defeat stress in the study of coping mechanisms and victimization. The initial operational definition of the socially defeated mouse by Ginsburg and Allee (1942) enabled the characterization of key endocrine, cardiovascular, and metabolic events during the initial response to an aggressive opponent and during the ensuing adaptations. Brief episodes of social defeat stress induce an augmented response to stimulant challenge as reflected by increased locomotion and increased extracellular dopamine (DA) in the nucleus accumbens (NAC). Cells in the ventral tegmental area (VTA) that project to the NAC were more active as indicated by increased expression of c-fos and Fos-immunoreactivity and BDNF. Intermittent episodes of social defeat stress result in increased mRNA for MOR in brainstem and limbic structures. These behavioral and neurobiological indices of sensitization persist for several months after the stress experience. The episodically defeated rats also self-administered intravenous cocaine during continuous access for 24 h (“binge”). By contrast, continuous social stress, particularly in the form of social subordination stress, leads to reduced appetite, compromised endocrine activities, and cardiovascular and metabolic abnormalities, and prefer sweets less as index of anhedonia. Cocaine challenges in subordinate rats result in a blunted psychomotor stimulant response and a reduced DA release in NAC. Subordinate rats self-administer cocaine less during continuous access conditions. These contrasting patterns of social stress result from continuous vs. intermittent exposure to social stress, suggesting divergent neuroadaptations for increased vulnerability to cocaine self-administration vs. deteriorated reward mechanisms characteristic of depressive-like profiles.

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Social conflict-induced changes in nociception and β-endorphin-like immunoreactivity in pituitary and discrete brain areas of C57BL/6 and DBA/2 mice

Cited by 41 publications

References 49 publications

Neuropeptide Regulation of the Locus Coeruleus and Opiate-Induced Plasticity of Stress Responses

Neuropeptide Regulation of the Locus Coeruleus and Opiate-Induced Plasticity of Stress Responses

Social stress, therapeutics and drug abuse: Preclinical models of escalated and depressed intake

Gene Expression in Aminergic and Peptidergic Cells During Aggression and Defeat: Relevance to Violence, Depression and Drug Abuse

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