Modulation of the Induction or Expression of Psychostimulant Sensitization by the Circumstances Surrounding Drug Administration

Robinson, Terry E.; Browman, Kaitlin E.; Crombag, Hans S.; Badiani, Aldo

doi:10.1016/s0149-7634(97)00020-1

Cited by 206 publications

(163 citation statements)

References 43 publications

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“…However, our results demonstrated that repeated injection of METH dosedependently induced behavioral sensitization in mice, and this effect lasted at least 3 weeks after the cessation of the drug treatment. These results are consistent with the findings that psychomotor stimulant-induced sensitization is not entirely dependent on drug-environment interactions [40]. The environmental context therefore does not appear to be critical for the induction of METH sensitization.…”

Section: Discussionsupporting

confidence: 90%

“…However, behavioral sensitization has been suggested as representing a conditioning phenomenon that is largely dependent on learned interactions between drug effects and environmental cues [40,45]. In this study, the induction of behavioral sensitization was performed in home cages and the expression of behavioral sensitization was measured in the locomotor arena.…”

Section: Discussionmentioning

confidence: 99%

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Attenuation of methamphetamine-induced behavioral sensitization in mice by systemic administration of naltrexone

Chiu

2005

Brain Research Bulletin

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Repeated intermittent exposure to psychostimulants was found to produce behavioral sensitization. The present study was designed to establish a mouse model and by which to investigate whether opioidergic system plays a role in methamphetamine-induced behavioral sensitization. Mice injected with 2.5 mg/kg of methamphetamine once a day for 7 consecutive days showed behavioral sensitization after challenge with 0.3125 mg/kg of the drug on day 11, whereas mice injected with a lower daily dose (1.25 mg/kg) did not. Mice received daily injections with either 1.25 or 2.5 mg/kg of methamphetamine showed behavioral sensitization after challenge with 1.25 mg/kg of the drug on days 11, 21, and 28. To investigate the role of opioidergic system in the induction and expression of behavioral sensitization, long-acting but non-selective opioid antagonist naltrexone was administrated prior to the daily injections of and challenge with methamphetamine, respectively. Our results show that the expressions of behavioral sensitization were attenuated by pretreatment with 10 or 20 mg/kg of naltrexone either during the induction period or before methamphetamine challenge when they were tested on days 11 and 21. These results indicate that repeated injection with methamphetamine dose-dependently induced behavioral sensitization in mice, and suggest the involvement of opioid receptors in the induction and expression of methamphetamine-induced behavioral sensitization.

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Section: Discussionsupporting

confidence: 90%

Section: Discussionmentioning

confidence: 99%

Attenuation of methamphetamine-induced behavioral sensitization in mice by systemic administration of naltrexone

Chiu

2005

Brain Research Bulletin

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“…The association of a novel environment to stimulant administration has a profound effect on the development of behavioral sensitization Crombag et al, 1996;Robinson et al, 1998). Seemingly in contrast to the findings described with CPP paradigms, Itzhak and Martin (2000) found that cocaine-induced place-dependent sensitization (context dependent), as measured by locomotor activity, was blocked by pretreatment with scopolamine (1 mg/kg s.c.).…”

Section: Acetylcholine and Conditioned Learningmentioning

confidence: 97%

The Role of Acetylcholine in Cocaine Addiction

Williams

Adinoff²

2007

Neuropsychopharmacol

160

138

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Central nervous system cholinergic neurons arise from several discrete sources, project to multiple brain regions, and exert specific effects on reward, learning, and memory. These processes are critical for the development and persistence of addictive disorders. Although other neurotransmitters, including dopamine, glutamate, and serotonin, have been the primary focus of drug research to date, a growing preclinical literature reveals a critical role of acetylcholine (ACh) in the experience and progression of drug use. This review will present and integrate the findings regarding the role of ACh in drug dependence, with a primary focus on cocaine and the muscarinic ACh system. Mesostriatal ACh appears to mediate reinforcement through its effect on reward, satiation, and aversion, and chronic cocaine administration produces neuroadaptive changes in the striatum. ACh is further involved in the acquisition of conditional associations that underlie cocaine self-administration and context-dependent sensitization, the acquisition of associations in conditioned learning, and drug procurement through its effects on arousal and attention. Long-term cocaine use may induce neuronal alterations in the brain that affect the ACh system and impair executive function, possibly contributing to the disruptions in decision making that characterize this population. These primarily preclinical studies suggest that ACh exerts a myriad of effects on the addictive process and that persistent changes to the ACh system following chronic drug use may exacerbate the risk of relapse during recovery. Ultimately, ACh modulation may be a potential target for pharmacological treatment interventions in cocaine-addicted subjects. However, the complicated neurocircuitry of the cholinergic system, the multiple ACh receptor subtypes, the confluence of excitatory and inhibitory ACh inputs, and the unique properties of the striatal cholinergic interneurons suggest that a precise target of cholinergic manipulation will be required to impact substance use in the clinical population.

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“…In this study it was found that the motor stimulant response elicited by cocaine was blunted by pretreatment of the nucleus accumbens with 6-cyano-7-nitroquinoxaline-2,3-dione only in animals receiving daily cocaine injections in the paired environment. In contrast, the N-methyl-D-aspartate glutamate receptor antagonist R-(-)-3-(2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid did not significantly affect cocaine-induced motor activity in any treatmentTo some extent, exploration beyond molecular binding of cocaine to dopamine transporters is impelled by a realization that the expression of behavioral adaptations to repeated cocaine is potently regulated by learned associations made between the pharmacological actions of the drug and environmental stimuli (Stewart and Vezina 1988;Robinson et al 1998). Thus, the daily administration of psychostimulant in a test environment produces more robust behavioral sensitization than when the drug is given in the home environment (Weiss et al 1989; Dietze and Kuschinsky 1994;Badiani et al 1997).…”

mentioning

confidence: 99%

Context-specific Enhancement of Glutamate Transmission by Cocaine

Bell

Duffy

Kalivas

2000

Neuropsychopharmacology

131

120

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The repeated injection of cocaine causes an increase in the capacity of a subsequent acute injection to elevate extracellular glutamate levels in the nucleus accumbens, and the present study sought to determine if the elevation in extracellular glutamate is regulated by the pairing of environmental stimuli with drug administration. Three treatment groups were injected daily for seven days with saline or cocaine (15 mg/kg, ip); 1) injection of saline in the home cage, 2) injection of cocaine in the home cage (cocaineunpaired), and 3) injection of cocaine in the test apparatus (cocaine-paired). Three weeks following the last daily injection dialysis probes were placed into the nucleus accumbens and all rats were injected with saline followed by cocaine. Basal levels of extracellular glutamate were significantly reduced in the cocaine-paired treatment group. The repeated administration of amphetamine-like psychostimulants produces enduring alterations in the behavioral response to subsequent drug administration. The behavioral adaptations include the induction of paranoia in humans, which has been modeled in rodents as the induction of a sensitized motor stimulant response to psychostimulant injection (Kokkinidis and Anisman 1980;Segal and Schuckit 1983;Robinson and Becker 1986). This animal model has been extensively employed over the last decade to elucidate the cellular adaptations that underlie the behavioral changes associated with repeated psychostimulant use. The research effort has been guided by two facts; 1) a critical molecular site of action for amphetamine-like psychostimulants is the dopamine transporter (Reith et al. 1986;Ritz et al. 1990; although see Rocha et al. 1998), and 2) dopa- NO . 3 mine transmission in the mesocorticolimbic dopamine projection from the ventral tegmental area to the nucleus accumbens is critical for the rewarding and motor stimulant actions of this class of drugs (Koob et al. 1993). Knowledge of the molecular action has precipitated the discovery of many cocaine-induced, dopamine-dependent neuroadaptations in the nucleus accumbens (see Nestler et al. 1993; White and Kalivas 1998, for reviews). Arising from this considerable research effort is the awareness that neither the emphasis on dopamine transmission nor the focus on the nucleus accumbens provides a complete profile of the neuroadaptations produced by repeated cocaine (Pierce and Kalivas 1997;Bardo 1998;Wolf 1998). Moreover, only in the cocaine-paired group did the cocaine injection elevate extracellular glutamate. Repeated administration of cocaine also produces an enduring increase in the motor stimulant response to an acute cocaine injection and it was previously found that administration of the ␣ -amino-3-hydroxy-5-methylisoxazole-4-propionic acid and kainic acid glutamate receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione inhibited the sensitized, but not the acute motor, response to cocaine. In this study it was found that the motor stimulant response elicited by cocaine was blunted by pretreatment of t...

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Modulation of the Induction or Expression of Psychostimulant Sensitization by the Circumstances Surrounding Drug Administration

Cited by 206 publications

References 43 publications

Attenuation of methamphetamine-induced behavioral sensitization in mice by systemic administration of naltrexone

Attenuation of methamphetamine-induced behavioral sensitization in mice by systemic administration of naltrexone

The Role of Acetylcholine in Cocaine Addiction

Context-specific Enhancement of Glutamate Transmission by Cocaine

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