How does stress increase risk of drug abuse and relapse?

Sinha, Rajita

doi:10.1007/s002130100917

Cited by 1,396 publications

(1,233 citation statements)

References 262 publications

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“…Pharmacological analysis suggests that blockade of a 2 -adrenoceptors plays a pertinent role in the ability of yohimbine to reinstate cocaine seeking and that dopaminergic mechanisms do not contribute critically to yohimbine-induced reinstatement of cocaine-seeking behavior. Stress has been implicated frequently as a factor underlying relapse to drug use among human drug abusers (Kreek and Koob, 1998;Sinha, 2001). Most clinical studies of the relationship between stress and relapse rely on either retrospective or prospective interviews, which are subject to the failures and distortion of recall (Hall et al, 1991;McKay et al, 1995).…”

Section: Discussionmentioning

confidence: 99%

“…Although stress has been implicated as a risk factor in drug addiction and relapse (Kreek and Koob, 1998;Sinha, 2001), the mechanisms by which stress triggers persistent drug seeking are still poorly understood (Sinha, 2001). There is, however, a growing body of literature linking activation of noradrenergic transmission to the behavioral and physiological consequences of stress (Stanford, 1995;Bremner et al, 1996).…”

Section: Introductionmentioning

confidence: 99%

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Pharmacological Blockade of α2-Adrenoceptors Induces Reinstatement of Cocaine-Seeking Behavior in Squirrel Monkeys

Lee

Tiefenbacher

Platt

et al. 2004

Neuropsychopharmacol

150

148

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Converging evidence suggests a role for noradrenergic mechanisms in stress-induced reinstatement of cocaine seeking in animals. Yohimbine, an a 2 -adrenoceptor antagonist, is known to be anxiogenic and induce stress-related responses in humans and animals. Here, we tested the ability of yohimbine to reinstate cocaine-seeking behavior and induce behavioral and physiological signs characteristic of stress in squirrel monkeys. Monkeys were trained to self-administer cocaine under a second-order schedule of i.v. drug injection. Drug seeking subsequently was extinguished by substituting saline for cocaine injections and omitting the cocaine-paired stimulus. The ability of yohimbine and the structurally distinct a 2 -adrenoceptor antagonist RS-79948 to reinstate cocaine-seeking behavior was assessed by administering priming injections immediately before test sessions in which the cocaine-paired stimulus was either present or absent. Priming injections of yohimbine (0.1-0.56 mg/kg, i.m.) or RS-79948 (0.01-0.1 mg/kg, i.m.) induced dose-related reinstatement of cocaineseeking behavior. The magnitude of yohimbine-induced reinstatement was similar regardless of the presence or absence of the cocainepaired stimulus. Yohimbine also significantly increased salivary cortisol levels, a physiological marker of stress, as well as scratching and selfgrooming, behavioral markers of stress in nonhuman primates. In drug interaction experiments, pretreatment with the a 2 -adrenoceptor agonist clonidine (0.1-0.3 mg/kg, i.m.) dose-dependently inhibited yohimbine-induced reinstatement of cocaine seeking. In contrast, pretreatment with the dopamine receptor antagonist flupenthixol failed to inhibit yohimbine-induced reinstatement of cocaine seeking. The results show that pharmacological blockade of a 2 -adrenoceptors can induce reinstatement of cocaine-seeking behavior and characteristic stress responses in squirrel monkeys, providing a potentially useful model of stress-induced relapse to drug seeking.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Pharmacological Blockade of α2-Adrenoceptors Induces Reinstatement of Cocaine-Seeking Behavior in Squirrel Monkeys

Lee

Tiefenbacher

Platt

et al. 2004

Neuropsychopharmacol

150

148

View full text Add to dashboard Cite

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“…For example, psychological stress elevates drug cravings (Sinha et al, 1999), and stress-induced hypothalamic-pituitary-adrenal (HPA) axis responses predict amounts of subsequent drug use (Sinha et al, 2006). Drugs of abuse themselves, and withdrawal from such drugs, can act as stressors promoting persistent and compulsive drug abuse (see reviews by Kreek and Koob, 1998;Stewart, 2000;Sinha, 2001). Furthermore, stressrelated anxiety and depression are major psychiatric consequences of chronic drug abuse, especially during withdrawal (Koob and le Moal, 1997;Markou et al, 1998).…”

Section: Introductionmentioning

confidence: 99%

Involvement of Arginine Vasopressin and V1b Receptor in Heroin Withdrawal and Heroin Seeking Precipitated by Stress and by Heroin

Zhou

Leri

Cummins

et al. 2007

Neuropsychopharmacol

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A previous study has shown that the stress responsive neurohormone arginine vasopressin (AVP) is activated in the amygdala during early withdrawal from cocaine. The present studies were undertaken to determine whether (1) AVP mRNA levels in the amygdala or hypothalamus, as well as hypothalamic-pituitary-adrenal (HPA) activity, would be altered during chronic intermittent escalating heroin administration (10 days; 7.5-60 mg/kg/day) or during early (12 h) and late (10 days) spontaneous withdrawal; (2) foot shock stress would alter AVP mRNA levels in the amygdala or hypothalamus in rats withdrawn from heroin self-administration (7 days, 3 h/day, 0.05 mg/kg/ infusion); and (3) the selective V1b receptor antagonist SSR149415 (1 and 30 mg/kg, intraperitoneal) would alter heroin seeking during tests of reinstatement induced by foot shock stress and by heroin primes (0.25 mg/kg), as well as HPA hormonal responses to foot shock. We found that AVP mRNA levels were increased during early spontaneous withdrawal in the amygdala only. This amygdalar AVP mRNA increase was no longer observed at the later stage of heroin withdrawal. Foot shock stress increased AVP mRNA levels in the amygdala of rats withdrawn from heroin self-administration, but not in heroin naïve rats. Behaviorally, SSR149415 dose-dependently attenuated foot shock-induced reinstatement and blocked heroin-induced reinstatement. Finally, SSR149415 blunted the HPA activation by foot shock. Together, these data in rats suggest that stress responsive AVP/V1b receptor systems (including the amygdala) may be critical components of the neural circuitry underlying the aversive emotional consequences of drug withdrawal, as well as the effect of negative emotional states on drug-seeking behavior.

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“…This is particularly surprising given the close association between stress and the vulnerability to substance abuse (Sinha, 2001;Soderpalm et al, 2003). Recent findings indicate that prior exposure to chronic unpredictable stress (CUS) enhances METH-associated toxicity to striatal DA terminals (Matuszewich and Yamamoto, 2004), but the underlying mechanisms of this enhancement are unknown.…”

Section: Introductionmentioning

confidence: 99%

Chronic stress enhances methamphetamine‐induced extracellular glutamate and excitotoxicity in the rat striatum

Tata

Yamamoto

2008

Synapse

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Striking parallels exist between the neurochemical and toxic effects of stress and methamphetamine. Despite these similarities, no studies have examined how stress may promote the toxic effects of methamphetamine (METH). The current study tested the hypothesis that chronic stress enhances METH toxicity by augmenting glutamate (GLU) release and excitotoxicity in response to METH administration. Adult male Sprague-Dawley rats were exposed to 10 days of unpredictable stress and then received either saline or METH (7.5 mg/kg, i.p., once every 2 h × four injections). Prior exposure to unpredictable stress acutely enhanced the striatal extracellular GLU concentrations in response to METH, and eventually caused proteolysis of the cytoskeleton protein spectrin. Administration of the corticosterone synthesis inhibitor, metyrapone (25 mg/kg, i.p., prior to each stressor), during unpredictable stress attenuated the enhanced striatal GLU release in response to METH, blocked spectrin proteolysis, and attenuated METH-associated toxicity measured by long-term depletions in the dopamine and serotonin tissue content as well as depletions in dopamine and serotonin transporter immunoreactivity of the striatum. In summary, prior exposure to unpredictable stress enhances METH-induced elevations of GLU in the striatum, resulting in long-term excitotoxic damage and an augmentation of damage to dopamine and serotonin terminals. These studies provide a neurochemical basis for how stress contributes to the deleterious effects of METH abuse.

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How does stress increase risk of drug abuse and relapse?

Cited by 1,396 publications

References 262 publications

Pharmacological Blockade of α2-Adrenoceptors Induces Reinstatement of Cocaine-Seeking Behavior in Squirrel Monkeys

Pharmacological Blockade of α2-Adrenoceptors Induces Reinstatement of Cocaine-Seeking Behavior in Squirrel Monkeys

Involvement of Arginine Vasopressin and V1b Receptor in Heroin Withdrawal and Heroin Seeking Precipitated by Stress and by Heroin

Chronic stress enhances methamphetamine‐induced extracellular glutamate and excitotoxicity in the rat striatum

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