The pedunculopontine tegmental nucleus and the role of cholinergic neurons in nicotine self-administration in the rat: a correlative neuroanatomical and behavioral study

Lança, A.J.; Adamson, K. L.; Coen, Kathleen M.; Chow, Brandon; Corrigall, William A.

doi:10.1016/s0306-4522(99)00607-7

Cited by 106 publications

(75 citation statements)

References 62 publications

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“…Interestingly, nAChRs in the VTA play a more important role than those in the nucleus accumbens in the effects of nicotine on the release of nucleus accumbens dopamine ( Nisell et al 1997). Consistent with these neurochemical data, behavioural data indicated that injections of the competitive nAChR antagonist DHbE into the VTA but not into the nucleus accumbens (Corrigall et al 1994), or lesions of the mesolimbic dopaminergic projections from the VTA to the nucleus accumbens (Corrigall et al 1992), or cholinergic lesions of the brainstem pedunculopontine nucleus that projects to the VTA (Lança et al 2000), or systemic administration of dopamine receptor antagonists (Corrigall & Coen 1991) decreased intravenous nicotine selfadministration in rats. In terms of nAChR subtypes, studies suggest an involvement of a4b2-containing nAChR subtypes in both the nicotine-induced release of dopamine and nicotine reinforcement (Picciotto et al 1998).…”

Section: Neurosubstrates Of Nicotine Reward Dependence and Withdrawalsupporting

confidence: 68%

Neurobiology of nicotine dependence

Markou

2008

Phil. Trans. R. Soc. B

236

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 Withdrawalsupporting

confidence: 68%

Neurobiology of nicotine dependence

Markou

2008

Phil. Trans. R. Soc. B

236

186

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“…Moreover, the ability of ghrelin administered into the LDTg to increase accumbal dopamine is attenuated by blockade of nAChRs in the VTA (Jerlhag et al, 2008). Collectively these data indicate that the socalled "cholinergic-dopaminergic reward link", a circuit conferring the incentive value of natural and artificial rewards (Yeomans et al, 1993, Lanca et al, 2000, Rada et al, 2000, Larsson and Engel, 2004, is a potential target for ghrelin's effects on the reward system.…”

Section: Introductionmentioning

confidence: 84%

Blockade of central nicotine acetylcholine receptor signaling attenuate ghrelin-induced food intake in rodents

et al. 2010

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“…While basic circuits underlying nicotine reinforcement have been extensively investigated Corrigall et al 1994;Corrigall et al 1992;Corrigall and Coen 1991;Jose Lanca et al 2000;Lanca et al 2000), only limited research has been conducted on the neural underpinnings for the interactions between nicotine and nonpharmacological stimuli (Liu et al 2004;Cohen et al 2005;Paterson et al 2005). The present paradigm has potential utility in such investigations, because it provides a means to dissociate the primary reinforcing and reinforcement-enhancing effects of nicotine.…”

Section: Discussionmentioning

confidence: 99%

Complex interactions between nicotine and nonpharmacological stimuli reveal multiple roles for nicotine in reinforcement

et al. 2005

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Although considerable progress has been made we do not yet fully understand the behavioral and neurobiological bases of nicotine reinforcement, and without this knowledge treatment strategies aimed at reducing smoking remain deficient. This dissertation provides an original perspective on nicotine reinforcement, which arises from substantial evidence of complex interactions between nicotine and nonpharmacological stimuli. The present experiments tested the hypothesis that nicotine reinforcement derives from at least two sources: 1) the primary reinforcing properties of nicotine, an action that requires response-dependent drug administration, and 2) the more prominent ability of nicotine to enhance behavior maintained by salient non-nicotine stimuli, an action that does not require a contingent relationship between drug administration and reinforced operant responding. Although novel for nicotine, this hypothesis has origins in an extensive literature on the reinforcing properties of psychostimulant drugs. Empirical support for the application of this hypothesis to nicotine reinforcement will be presented. By investigating the interaction between nicotine and nonpharmacological stimuli within the context of drug selfadministration in rats, the present research has generated new insights into the paradox of how nicotine, an apparently weak primary reinforcer, can sustain the robust behavior observed in selfadministration and in smoking. Hypotheses generated by these data provide important direction for future investigations into the neurobiology of nicotine reinforcement.iii

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The pedunculopontine tegmental nucleus and the role of cholinergic neurons in nicotine self-administration in the rat: a correlative neuroanatomical and behavioral study

Cited by 106 publications

References 62 publications

Neurobiology of nicotine dependence

Neurobiology of nicotine dependence

Blockade of central nicotine acetylcholine receptor signaling attenuate ghrelin-induced food intake in rodents

Complex interactions between nicotine and nonpharmacological stimuli reveal multiple roles for nicotine in reinforcement

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