Conditioned place aversion to the “hangover” phase of acute ethanol administration in the rat

Morse, Andrew C.; Schulteis, Gery; Holloway, Frank; Koob, George F.

doi:10.1016/s0741-8329(00)00099-9

Cited by 48 publications

(43 citation statements)

References 37 publications

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“…The emotional components of withdrawal include dissociable signs of anxiety and dysphoria (Rothwell et al, 2009). Anxiety-like increases in startle magnitude are seen after acute exposure to morphine (Harris and Gewirtz, 2004), as well as nicotine (Engelmann et al, 2009), whereas dysphoria may be indicated by conditioned place aversions that develop with a delay following acute exposure to opiates (Bechara et al, 1995;Pain et al, 2008), cocaine (Ettenberg and Bernardi, 2007;Pliakas et al, 2001), and ethanol (Morse et al, 2000). Increased thresholds for intracranial self-stimulation are also a common feature of withdrawal from most abused drugs (Koob et al, 2004).…”

Section: Discussionmentioning

confidence: 99%

Episodic Withdrawal Promotes Psychomotor Sensitization to Morphine

Rothwell

Gewirtz

Thomas

2010

Neuropsychopharmacol

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The relative intermittency or continuity of drug delivery is a major determinant of addictive liability, and also influences the impact of drug exposure on brain function and behavior. Events that occur during the offset of drug action (ie, acute withdrawal) may have an important role in the consequences of intermittent drug exposure. We assessed whether recurrent episodes of acute withdrawal contribute to the development of psychomotor sensitization in rodents during daily morphine exposure. The acoustic startle reflexFa measure of anxiety induced by opiate withdrawalFwas used to resolve and quantify discrete withdrawal episodes, and pharmacological interventions were used to manipulate withdrawal severity. Startle potentiation was observed during spontaneous withdrawal from a single morphine exposure, and individual differences in initial withdrawal severity positively predicted the subsequent development of sensitization. Manipulations that reduce or exacerbate withdrawal severity also produced parallel changes in the degree of sensitization. These results demonstrate that the episodic experience of withdrawal during daily drug exposure has a novel role in promoting the development of psychomotor sensitizationFa prominent model of drug-induced neurobehavioral plasticity. Episodic withdrawal may have a pervasive role in many effects of intermittent drug exposure and contribute to the development of addiction.

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Section: Discussionmentioning

confidence: 99%

Episodic Withdrawal Promotes Psychomotor Sensitization to Morphine

Rothwell

Gewirtz

Thomas

2010

Neuropsychopharmacol

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“…Ten hours later, we placed the rats in the center of an elevated plus maze and allowed them to explore the closed and open arms of the apparatus for a 5 min period. Previous experiments (Morse et al, 2000) showed that BALs are undetectable 10 h after bolus injection of 3 g/kg ethanol. Thirty minutes before anxiety testing, separate groups of rats were injected with one of several doses of gabapentin (0, 30, 60, or 120 mg/kg, i.p; n ϭ 8 -10 per dose).…”

Section: Behavioral Studiesmentioning

confidence: 90%

Cellular and Behavioral Interactions of Gabapentin with Alcohol Dependence

Roberto¹,

Gilpin²,

O’Dell³

et al. 2008

J. Neurosci.

118

128

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Gabapentin is a structural analog of GABA that has anticonvulsant properties. Despite the therapeutic efficacy of gabapentin, its molecular and cellular mechanisms of action are unclear. The GABAergic system in the central nucleus of the amygdala (CeA) plays an important role in regulating voluntary ethanol intake. Here, we investigated the effect of gabapentin on GABAergic transmission in CeA slices, on ethanol intake, and on an anxiety measure using animal models of ethanol dependence. Gabapentin increased the amplitudes of evoked GABA receptor-mediated IPSCs (GABA-IPSCs) in CeA neurons from nondependent rats, but decreased their amplitudes in CeA of ethanol-dependent rats. Gabapentin effects were blocked in the presence of a specific GABA B receptor antagonist. The sensitivity of the GABA-IPSCs to a GABA B receptor antagonist and an agonist was decreased after chronic ethanol, suggesting that ethanol-induced neuroadaptations of GABA B receptors associated with ethanol dependence may account for the differential effects of gabapentin after chronic ethanol. Systemic gabapentin reduced ethanol intake in dependent, but not in nondependent, rats and reversed the anxiogeniclike effects of ethanol abstinence using an acute dependence model. Gabapentin infused directly into the CeA also blocked dependenceinduced elevation in operant ethanol responding. Collectively, these findings show that gabapentin reverses behavioral measures of ethanol dependence and, in turn, dependence reverses the effects of gabapentin on CeA neurons, and suggest that gabapentin represents a potential medication for treatment of alcoholism.

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“…), adult male rats present a reduced exploration of the open arms in the elevated plus maze (Doremus et al, 2003), and significant social suppression in the social interaction test (Varlinskaya and Spear, 2004), a response pattern that is consistent with an anxiogenic profile (File et al, 1976;Pellow et al, 1985). Moreover, Morse et al (2000) have demonstrated that the hangover following an acute injection of high doses of ethanol (3-4 g/kg) produces a significant conditioned place aversion in the rat. Contrasting with these results, Gauvin et al (1997) have demonstrated that although acute administration of high ethanol doses, most typically, induces conditioned place aversions, the repeated pairing of ethanol hangover with the initially nonpreferred side of the chambers results in the development of a conditioned place preference in rats, suggesting that, in some cases, the hangover procedure did not induce aversive response.…”

Section: Introductionmentioning

confidence: 91%

Activation of Adenosine A1 Receptors Reduces Anxiety-Like Behavior During Acute Ethanol Withdrawal (Hangover) in Mice

Prediger

Silva

Batista

et al. 2006

Neuropsychopharmacol

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Elevated signs of anxiety are observed in both humans and rodents during withdrawal from chronic as well as acute ethanol exposure, and it represents an important motivational factor for ethanol relapse. Several reports have suggested the involvement of brain adenosine receptors in different actions produced by ethanol such as motor incoordination and hypnotic effects. In addition, we have recently demonstrated that adenosine A 1 receptors modulate the anxiolytic-like effect induced by ethanol in mice. In the present study, we evaluated the potential of adenosine A 1 and A 2A receptor agonists in reducing the anxiety-like behavior during acute ethanol withdrawal (hangover) in mice. Animals received a single intraperitoneal administration of saline or ethanol (4 g/kg) and were tested in the elevated plus maze after an interval of 0.5-24 h. The results indicated that hangover-induced anxiety was most pronounced between 12 and 18 h after ethanol administration, as indicated by a significant reduction in the exploration of the open arms of the maze. At this time interval, ethanol was completely cleared. The acute administration of 'nonanxiolytic' doses of adenosine and the selective adenosine A 1 receptor agonist 2-chloro-N6-cyclopentyladenosine (CCPA), but not the adenosine A 2A receptor agonist N6-[2-(3,5-dimethoxyphenyl)-2-(2-methylphenyl)ethyl]adenosine (DPMA), at the onset of peak withdrawal (18 h), reduced this anxiogenic-like response. In addition, the effect of CCPA on the anxiety-like behavior of ethanol hangover was reversed by pretreatment with the selective adenosine A 1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX). These results reinforce the notion of the involvement of adenosine receptors in the anxiety-like responses and indicate the potential of adenosine A 1 receptor agonists to reduce the anxiogenic effects during ethanol withdrawal.

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Conditioned place aversion to the “hangover” phase of acute ethanol administration in the rat

Cited by 48 publications

References 37 publications

Episodic Withdrawal Promotes Psychomotor Sensitization to Morphine

Episodic Withdrawal Promotes Psychomotor Sensitization to Morphine

Cellular and Behavioral Interactions of Gabapentin with Alcohol Dependence

Activation of Adenosine A1 Receptors Reduces Anxiety-Like Behavior During Acute Ethanol Withdrawal (Hangover) in Mice

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