The GABA B receptor agonists baclofen and CGP44532 decreased nicotine self-administration in the rat

Paterson, Neil E.; Froestl, Wolfgang; Markou, Athina

doi:10.1007/s00213-003-1637-1

Cited by 124 publications

(115 citation statements)

References 39 publications

(54 reference statements)

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“…The issue of tolerance is important because drug therapies currently need to be administered chronically to humans for smoking cessation. However, in studies of rats, GVG and GABA B receptor agonists also decreased responding for food, although at higher doses than the threshold doses for inducing decreases in nicotine selfadministration (Paterson & Markou 2002;Paterson et al 2004Paterson et al , 2005b figure 4a). These effects on responding for food may reflect non-specific performance effects of the GABAergic compounds or specific effects on food intake.…”

Section: Neurosubstrates Of Nicotine Reward Dependence and Withdrawalmentioning

confidence: 98%

“…Both GABA A and GABA B receptors are inhibitory and both are found presynaptically and postsynaptically. Systemic injections or microinjections of baclofen or CGP44532 [(3-amino-2[S ]-hydroxypropyl)-methylphosphonic acid], two GABA B receptor agonists, into the nucleus accumbens shell, VTA or pedunculopontine tegmental nucleus that sends cholinergic, GABAergic and glutamatergic projections to the VTA (but not injections into the caudate-putamen) decreased the reinforcing effects of nicotine (Shoaib et al 1998;Corrigall et al 2000Corrigall et al , 2001Fattore et al 2002;Paterson et al 2004; figure 4a). These decreases in nicotine self-administration persisted even after chronic administration of CGP44532 for 14 days, indicating little tolerance to this effect of the GABA B receptor agonist with this length of treatment (Paterson et al 2005b).…”

Section: Neurosubstrates Of Nicotine Reward Dependence and Withdrawalmentioning

confidence: 99%

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Neurobiology of nicotine dependence

Markou

2008

Phil. Trans. R. Soc. B

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232

186

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Nicotine is a psychoactive ingredient in tobacco that significantly contributes to the harmful tobacco smoking habit. Nicotine dependence is more prevalent than dependence on any other substance. Preclinical research in animal models of the various aspects of nicotine dependence suggests a critical role of glutamate, g-aminobutyric acid (GABA), cholinergic and dopamine neurotransmitter interactions in the ventral tegmental area and possibly other brain sites, such as the central nucleus of the amygdala and the prefrontal cortex, in the effects of nicotine. Specifically, decreasing glutamate transmission or increasing GABA transmission with pharmacological manipulations decreased the rewarding effects of nicotine and cue-induced reinstatement of nicotine seeking. Furthermore, early nicotine withdrawal is characterized by decreased function of presynaptic inhibitory metabotropic glutamate 2/3 receptors and increased expression of postsynaptic glutamate receptor subunits in limbic and frontal brain sites, while protracted abstinence may be associated with increased glutamate response to stimuli associated with nicotine administration. Finally, adaptations in nicotinic acetylcholine receptor function are also involved in nicotine dependence. These neuroadaptations probably develop to counteract the decreased glutamate and cholinergic transmission that is hypothesized to characterize early nicotine withdrawal. In conclusion, glutamate, GABA and cholinergic transmission in limbic and frontal brain sites are critically involved in nicotine dependence.

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Section: Neurosubstrates Of Nicotine Reward Dependence and Withdrawalmentioning

confidence: 98%

Section: Neurosubstrates Of Nicotine Reward Dependence and Withdrawalmentioning

confidence: 99%

Neurobiology of nicotine dependence

Markou

2008

Phil. Trans. R. Soc. B

Self Cite

232

186

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“…Preclinical studies with rodents have suggested that administration of GABA B agonists including baclofen and GABA B -positive receptor modulators have anti-motivational effects and decreases self-administration of nicotine (Fattore et al, 2002;Paterson et al, 2004Paterson et al, , 2008, cocaine (Roberts et al, 1996;Brebner et al, 2002), methamphetamine, (Ranaldi and Poeggel, 2002), and heroin (Spano et al, 2007).…”

Section: Baclofenmentioning

confidence: 99%

Novel Therapeutic Strategies for Alcohol and Drug Addiction: Focus on GABA, Ion Channels and Transcranial Magnetic Stimulation

Addolorato

Leggio

Hopf

et al. 2011

Neuropsychopharmacol

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Drug addiction represents a major social problem where addicts and alcoholics continue to seek and take drugs despite adverse social, personal, emotional, and legal consequences. A number of pharmacological compounds have been tested in human addicts with the goal of reducing the level or frequency of intake, but these pharmacotherapies have often been of only moderate efficacy or act in a sub-population of humans. Thus, there is a tremendous need for new therapeutic interventions to treat addiction. Here, we review recent interesting studies focusing on gamma-aminobutyric acid receptors, voltage-gated ion channels, and transcranial magnetic stimulation. Some of these treatments show considerable promise to reduce addictive behaviors, or the early clinical studies or pre-clinical rationale suggest that a promising avenue could be developed. Thus, it is likely that within a decade or so, we could have important new and effective treatments to achieve the goal of reducing the burden of human addiction and alcoholism.

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“…Either of two GABA B receptor agonists, (3-amino-2[S]-hydroxypropyl)-methylphosphinic acid (CGP44532) or baclofen, decreased self-administration of cocaine (Roberts et al, 1996;Shoaib et al, 1998;Brebner et al, 1999Brebner et al, , 2000aCorrigall et al, 2000;Di Ciano and Everitt, 2003;Campbell et al, 2002), methamphetamine (Ranaldi and Poeggel, 2002), heroin (Xi and Stein, 1999), alcohol (Colombo et al, , 2002, and nicotine (Corrigall et al, 2000(Corrigall et al, , 2001Fattore et al, 2002;Paterson et al, 2004) in rats. Further, baclofen decreased morphine-induced locomotor stimulation (Leite-Morris et al, 2002) and methamphetamine-induced conditioned place preference (Li et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

“…Second, the long time course (5-10 days) of extinction of nicotineseeking behavior seen in some studies (Corrigall and Coen, 1989;Donny et al, 1995;Chiamulera et al, 1996;Shaham et al, 1997;however, see Watkins et al, 1999) suggested that the effects of acute vs repeated administration of CGP44532 could differ. Two doses of CGP44532 were selected based on previous work (Paterson et al, 2004); one dose that nonselectively decreased nicotine-and foodmaintained responding (0.5 mg/kg) and another dose (0.25 mg/kg) that had no effect on either nicotine (0.03 mg/kg/infusion)-or food-maintained responding when administered acutely.…”

Section: Introductionmentioning

confidence: 99%

Repeated Administration of the GABAB Receptor Agonist CGP44532 Decreased Nicotine Self-Administration, and Acute Administration Decreased Cue-Induced Reinstatement of Nicotine-Seeking in Rats

Paterson

Froestl

Markou

2004

Neuropsychopharmacol

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Acute administration of g-aminobutyric acid B (GABA B ) receptor agonists decreased nicotine, cocaine, ethanol, and heroin selfadministration. GABA B receptor agonists also decreased cue-induced cocaine craving or seeking in humans and animals, respectively. The present study investigated the effects of repeated subcutaneous administration of the GABA B receptor agonist CGP44532 on nicotineand food-maintained responding under a fixed ratio 5 schedule of reinforcement. The second part of the study determined whether contingent presentation of previously nicotine-associated cues reinstated extinguished nicotine-seeking behavior, and whether acute subcutaneous CGP44532 administration affected cue-induced reinstatement of extinguished nicotine-seeking behavior. The results indicated that repeated administration of 0.25 mg/kg CGP44532 selectively decreased nicotine self-administration compared to foodmaintained responding during the first 7 days of treatment. Repeated administration of 0.5 mg/kg/day CGP44532 nonselectively decreased both nicotine-and food-maintained responding. Contingent presentation of previously nicotine-associated cues reinstated extinguished nicotine-seeking behavior. Further, acute CGP44532 administration (0.125 and 0.25 mg/kg) decreased cue-induced reinstatement of nicotine-seeking behavior. In summary, the present results indicated that 0.25 mg/kg/day CGP44532 selectively decreased nicotine self-administration compared to food-maintained responding, and acute administration of CGP44532 (0.125 and 0.25 mg/kg) dose-dependently decreased cue-induced reinstatement of nicotine-seeking behavior.

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The GABA B receptor agonists baclofen and CGP44532 decreased nicotine self-administration in the rat

Cited by 124 publications

References 39 publications

Neurobiology of nicotine dependence

Neurobiology of nicotine dependence

Novel Therapeutic Strategies for Alcohol and Drug Addiction: Focus on GABA, Ion Channels and Transcranial Magnetic Stimulation

Repeated Administration of the GABAB Receptor Agonist CGP44532 Decreased Nicotine Self-Administration, and Acute Administration Decreased Cue-Induced Reinstatement of Nicotine-Seeking in Rats

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