Involvement of Acetylcholine in the Nucleus Accumbens in Cocaine Reinforcement

Mark, Gregory P.; Kinney, Anthony E.; Grubb, Michele C.; Keys, Alan

doi:10.1111/j.1749-6632.1999.tb09324.x

Cited by 19 publications

(13 citation statements)

References 7 publications

(9 reference statements)

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“…None of the other neuron types in the accumbens corridor, i.e., cholinergic interneurons or the various GABAergic interneurons, were involved in the differential activation. In the case of the cholinergic interneurons, this was especially surprising to us, as we (Crespo et al, 2006, 2008, 2012), like many other groups (Wilson and Schuster, 1973; Acquas et al, 1996; Mark et al, 1999; Pratt and Kelley, 2004; Smith et al, 2004; Grasing et al, 2009; Witten et al, 2010; English et al, 2011; Cachope et al, 2012; De La Garza et al, 2012; Hikida et al, 2012; Threlfell et al, 2012) had provided evidence for the involvement of the accumbal cholinergic system in drug- and food reward and as cholinergic interneurons (Berlanga et al, 2003) were shown to be instrumental for the acquisition of cocaine CPP (Witten et al, 2010). Accordingly, we had demonstrated in a rat runway procedure that acetylcholine (ACh) release and activation of muscarinic and nicotinic ACh receptors were necessary for the acquisition of the rewarding properties of cocaine, of two pharmacokinetically very different μ opioid receptor agonists, i.e., remifentanil and morphine, and of highly palatable food (Crespo et al, 2006, 2008).…”

Section: Discussionmentioning

confidence: 55%

Reacquisition of cocaine conditioned place preference and its inhibition by previous social interaction preferentially affect D1-medium spiny neurons in the accumbens corridor

Prast

Schardl

Schwarzer

et al. 2014

Front. Behav. Neurosci.

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We investigated if counterconditioning with dyadic (i.e., one-to-one) social interaction, a strong inhibitor of the subsequent reacquisition of cocaine conditioned place preference (CPP), differentially modulates the activity of the diverse brain regions oriented along a mediolateral corridor reaching from the interhemispheric sulcus to the anterior commissure, i.e., the nucleus of the vertical limb of the diagonal band, the medial septal nucleus, the major island of Calleja, the intermediate part of the lateral septal nucleus, and the medial accumbens shell and core. We also investigated the involvement of the lateral accumbens core and the dorsal caudate putamen. The anterior cingulate 1 (Cg1) region served as a negative control. Contrary to our expectations, we found that all regions of the accumbens corridor showed increased expression of the early growth response protein 1 (EGR1, Zif268) in rats 2 h after reacquisition of CPP for cocaine after a history of cocaine CPP acquisition and extinction. Previous counterconditioning with dyadic social interaction inhibited both the reacquisition of cocaine CPP and the activation of the whole accumbens corridor. EGR1 activation was predominantly found in dynorphin-labeled cells, i.e., presumably D1 receptor-expressing medium spiny neurons (D1-MSNs), with D2-MSNs (immunolabeled with an anti-DRD2 antibody) being less affected. Cholinergic interneurons or GABAergic interneurons positive for parvalbumin, neuropeptide Y or calretinin were not involved in these CPP-related EGR1 changes. Glial cells did not show any EGR1 expression either. The present findings could be of relevance for the therapy of impaired social interaction in substance use disorders, depression, psychosis, and autism spectrum disorders.

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Section: Discussionmentioning

confidence: 55%

Reacquisition of cocaine conditioned place preference and its inhibition by previous social interaction preferentially affect D1-medium spiny neurons in the accumbens corridor

Prast

Schardl

Schwarzer

et al. 2014

Front. Behav. Neurosci.

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“…That is, the effects of nicotine are mediated by its activation of the mesolimbic system, resulting in an increase in dopamine (DA) output. Likewise, cocaine self-administration leads to an increased synaptic availability of DA and stimulates acetylcholine (ACH) release in the nucleus accumbens (NAc) that may activate acetylcholine receptors (AChRs) (Kalivas and Duffy, 1988;Mark et al, 1999). Joint administration of nicotine and cocaine, in fact, has been reported to have additive effects on NAc DA (Zernig et al, 1997;Gerasimov et al, 2000).…”

Section: Relationship To Addictive Behaviormentioning

confidence: 98%

Addiction and Dose Response: The Psychomotor Stimulant Theory of Addiction Reveals That Hormetic Dose Responses Are Dominant

Calabrese

2008

Critical Reviews in Toxicology

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In 1987 Wise and Bozarth proposed a psychomotor stimulant theory of addiction whose most consistent feature was enhanced forward (horizontal) locomotion. While controversial, the theory of Wise and Bozarth has had substantial impact on addiction behavior theory over the past two decades, being cited over 1,400 times. The present assessment places the theoretical formulation of Wise and Bozarth (1987) within a dose-response framework. This analysis demonstrates that the psychomotor stimulant effects of addictive drugs routinely display biphasic dose-response relationships that are consistent with the quantitative features of the hormetic dose-response model. This is the case, regardless of addictive agent, animal model, and experimental protocol employed. Not only do these findings suggest an important role for the hormetic dose response model in the assessment of addictive behaviors, they also further extend the generalizability of the hormesis dose-response model concept within the biomedical sciences.

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“…with the psychostimulant methylphenidate (Volkow and Swanson, 2003), or when nicotine calms 'agitated nerves' (Balfour, 1991). Physiologically, psychostimulants typically increase the functional activity of central monoaminergic and cholinergic systems (Fibiger and Phillips, 1988;Coury et al, 1992;Mark et al, 1999;Nestby et al, 1997), although this is not an exclusive property of psychostimulants, as many depressant drugs, such as alcohol (Katner and Weiss, 1999), are also powerful activators of these neurochemical substrates. Nevertheless, the use of the term 'psychostimulant' clearly has some descriptive value, and it encompasses a range of drugs that induce some common behavioral effects.…”

Section: Psychostimulant Drugsmentioning

confidence: 98%

Psychostimulant withdrawal as an inducing condition in animal models of depression

Barr

Markou

2005

Neuroscience & Biobehavioral Reviews

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Involvement of Acetylcholine in the Nucleus Accumbens in Cocaine Reinforcement

Cited by 19 publications

References 7 publications

Reacquisition of cocaine conditioned place preference and its inhibition by previous social interaction preferentially affect D1-medium spiny neurons in the accumbens corridor

Reacquisition of cocaine conditioned place preference and its inhibition by previous social interaction preferentially affect D1-medium spiny neurons in the accumbens corridor

Addiction and Dose Response: The Psychomotor Stimulant Theory of Addiction Reveals That Hormetic Dose Responses Are Dominant

Psychostimulant withdrawal as an inducing condition in animal models of depression

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