Anxiogenic properties of cocaine withdrawal

Wood, Douglas M.; Lal, Harbans

doi:10.1016/0024-3205(87)90619-9

Cited by 54 publications

(25 citation statements)

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“…In rats, cocaine can induce anxiety-like behaviors as measured in a number of pharmacological-animal models (Basso et al, 1999;Paine et al, 2002;Rogerio and Takahashi, 1992;Yang et al, 1992). The benzodiazepine, diazepam, can be effective in reducing cocaineinduced anxiety-like behavior (Ettenberg and Geist, 1991;Paine et al, 2002;Wood and Lal, 1987), however, the serotonergic agents, buspirone and SB 224289, are not (Hoplight et al, 2005;Paine et al, 2002).…”

Section: Discussionmentioning

confidence: 99%

Withdrawal from chronic administration of cocaine decreases delta opioid receptor signaling and increases anxiety- and depression-like behaviors in the rat

et al. 2008

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Chronic administration of cocaine has been shown to attenuate the functional capacity of delta opioid receptors to inhibit adenylyl cyclase activity. Abuse and withdrawal from cocaine in humans is associated with increases in anxiety and depression. Since recent research supports the role of delta opioid receptors in anxiety-and depression-like behaviors in rodents, we hypothesized that functional desensitization of delta opioid receptors contributes to anxiety-and depression-like behavioral phenotypes following short-term withdrawal from chronic administration of cocaine. To test this hypothesis, delta opioid receptor signaling and behaviors were evaluated 24 h after 14 days of bingepattern cocaine administration (15 mg/kg three times daily at 1 h intervals) in male Sprague Dawley rats. Results showed that the inhibition of adenylyl cyclase by delta opioid receptor agonists was attenuated in the frontal cortex, nucleus accumbens and caudate putamen 24 h after cessation of cocaine administration. One day withdrawal from chronic administration of cocaine resulted in increased anxiety-and depression-like behaviors as measured by the elevated plus maze and the force swim test respectively, and no change in locomotor activity. The anxiety-and depression-like behaviors were dose-dependently reduced by acute administration of the selective delta opioid receptor agonist, SNC80. These results demonstrate that early withdrawal from cocaine resulted in increased anxiety and depression, which accompanies the desensitization of delta opioid receptor function. Furthermore, cocaine-induced anxiety-and depression-like behaviors were reversible by the delta opioid receptor agonist SNC80.

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Section: Discussionmentioning

confidence: 99%

Withdrawal from chronic administration of cocaine decreases delta opioid receptor signaling and increases anxiety- and depression-like behaviors in the rat

et al. 2008

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Section: Concerns Of Validity: Are We Really Measuringmentioning

confidence: 92%

“…Subsequently, a series of studies characterized the discriminative stimulus effects of PTZ in rats during withdrawal from a number of drugs of abuse, including diazepam, morphine, cocaine, and nicotine [Emmett-Oglesby et al, 1984, 1988Harris et al, 1986;Wood and Lal, 1987]. In each case, substantial PTZ responding was observed during withdrawal, suggesting that at least some of the anxiety produced by drug withdrawal is mediated via GABA A systems.…”

Section: Operant Models Of Anxietymentioning

confidence: 98%

“…Cocaine has been reported to substitute for PTZ in some studies Lal, 1979, 1981] but not in others [Prather and Lal, 1992;Wood and Lal, 1987]. In addition, chronic administration of cocaine increased responding to both lower doses of PTZ and to cocaine [Wood and Lal, 1987]. Likewise, diazepam blocked PTZ-lever responding during withdrawal from cocaine and during protracted EW (up to 5 days after removal of ethanol), cocaine produced higher levels of PTZ-lever responding than in nondependent rats [Prather and Lal, 1992].…”

Section: Concerns Of Validity: Are We Really Measuringmentioning

confidence: 99%

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Animal models of the anxiogenic effects of ethanol withdrawal

Gatch¹,

Lal²

2001

Drug Development Research

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Although anxiety is a major feature of ethanol withdrawal (EW) and much of treatment related to EW is focused on amelioration of the anxiety experienced during EW, less attention has been given to the anxiogenic effects of EW than to the convulsant effects. In this article, we review the animal literature on the anxiogenic effects of EW. Both GABA A and serotonin (5-HT) receptors are important targets in the treatment of anxiety. The roles of each of these two receptors on the anxiogenic effects of EW as well as their potential interrelation are discussed. The contribution of other receptor systems to the modulation of these effects is reviewed. Additionally, males and females show very different levels of anxiety during EW and studies on the role of the HPA axis in mediating these effects are examined. Finally, potential directions for better treatments for EW are discussed. Drug Dev. Res. 54:95-115, 2001.

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“…Cocaine is not only euphorigenic, but also can produce anxiety in humans and anxiety-like behavioral effects in animals (Blanchard and Blanchard, 1999;Ettenberg, 2004) following both acute and chronic administration (Yang et al, 1992) as well as during cocaine withdrawal (Wood and Lal, 1987). In addition, cocaine-associated cues were shown to produce anxiety-like behavior in rats after systemic administration of cocaine (DeVries and Pert, 1998).…”

Section: Introductionmentioning

confidence: 99%

Subchronic Cannabinoid Agonist (WIN 55,212-2) Treatment during Cocaine Abstinence Alters Subsequent Cocaine Seeking Behavior

González-Cuevas

Aujla

Martin‐Fardon

et al. 2007

Neuropsychopharmacol

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The co-abuse of marijuana with cocaine is widespread, but it has not been until recently that the relationship between the behavioral effects of cannabinoids and cocaine has begun to be unveiled in animal models. Male Wistar rats were trained to intravenously selfadminister cocaine until a stable baseline was reached. Rats then were subjected to a 5-day cocaine deprivation period during which they were treated daily with the cannabinoid receptor agonist WIN 55,212-2 (R-( + )-[2,3-dihydro-5-methyl-3-(4-morpholinylmethyl)pyrrolo[1,2,3-de]-1,4-benzoxazin-6-yl]-1-naphthalenylmethanone mesylate) (0, 0.3, 1, and 3 mg/kg; i.p.). Following this subchronic treatment, rats were tested, in counterbalanced order, in a test of anxiety (elevated plus-maze), as well as extinction and cue-induced reinstatement tests, the latter conducted according to a between-within procedure. Subchronic administration of WIN 55,212-2 was found to produce dose-dependent alterations of performance in the extinction, reinstatement, and anxiety tests with the lowest dose of WIN 55,212-2 producing the highest resistance to extinction and reinstatement, and the highest dose of WIN 55,212-2 producing the highest anxiolytic activity. Subchronic treatment with WIN 55,212-2 in rats without a history of cocaine self-administration did not affect anxiety levels. The results suggest an important role of the cannabinoid system in neuronal processes underlying cocaine seeking behavior. However, further studies will be necessary to understand possible implications of these findings for a role of the cannabinoid system as a treatment target for human cocaine abuse.

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Anxiogenic properties of cocaine withdrawal

Cited by 54 publications

References 10 publications

Withdrawal from chronic administration of cocaine decreases delta opioid receptor signaling and increases anxiety- and depression-like behaviors in the rat

Withdrawal from chronic administration of cocaine decreases delta opioid receptor signaling and increases anxiety- and depression-like behaviors in the rat

Animal models of the anxiogenic effects of ethanol withdrawal

Subchronic Cannabinoid Agonist (WIN 55,212-2) Treatment during Cocaine Abstinence Alters Subsequent Cocaine Seeking Behavior

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