Cholinergic modulation of dopamine pathways through nicotinic acetylcholine receptors

Kloet, Sybren F. de; Mansvelder, Huibert D.; Vries, Taco J. De

doi:10.1016/j.bcp.2015.07.014

Cited by 56 publications

(33 citation statements)

References 229 publications

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“…Family-based association testing showed that rs1044396 of the CHRNA4 gene was significantly associated with a protective effect against nicotine addiction [ 21 ], similar to our results. One possible explanation for the effect of the CHRNA4 gene on addiction is that the cholinergic pathway is involved in actions in the mesolimbic dopaminergic system, which serves a principal role in the acquisition of addictive behavior [ 53 ]. Nearly all ventral tegmental area (VTA) DA neurons display an Ach-induced current with α4β2-type nicotinic acetylcholine receptors (nAchRs) and the activation of the α4 subunit is especially important for the modulation of nicotine-induced reward, sensitization, and tolerance [ 54 ].…”

Section: Discussionmentioning

confidence: 99%

The association between the nicotinic acetylcholine receptor α4 subunit gene (CHRNA4) rs1044396 and Internet gaming disorder in Korean male adults

et al. 2017

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The primary aim of this study was to investigate the genetic predisposition of Internet gaming disorder (IGD), and the secondary aim was to compare the results to those of alcohol dependence (AD). Two independent case-control studies were conducted. A total of 30 male participants with IGD, diagnosed according to the 5th edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) criteria, and 30 sex-matched controls participated in study 1. We designed targeted exome sequencing (TES) to test for 72 candidate genes that have been implicated in the pathogenesis of addiction. The genes included seven neurotransmitter (dopamine, serotonin, glutamate, r-aminobutyric acid (GABA), norepinephrine, acetylcholine, and opioid) system genes. A total of 31 male in-patients with AD and 29 normal male controls (NC) were enrolled in study 2. The same 72 genes included in study 1 and ten additional genes related to alcohol-metabolic enzyme were selected as the target genes, and we identified the genetic variants using the same method (TES). The IGD group had a lower frequency of the allele of rs1044396 in the nicotinic acetylcholine receptor alpha 4 subunit (CHRNA4), and this variant represents a protective allele against IGD. However, we did not find a significant difference in the polymorphisms of the 72 genes that encode neurotransmitter systems between the AD and NC groups. This study demonstrated that rs1044396 of CHRNA4 was significantly associated with IGD.

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Section: Discussionmentioning

confidence: 99%

The association between the nicotinic acetylcholine receptor α4 subunit gene (CHRNA4) rs1044396 and Internet gaming disorder in Korean male adults

et al. 2017

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“…Accordingly, these data obtained by optogenetic manipulation of the VTA dopaminergic neurons provide strong evidence for a causal relationship with forced swim performance. The VTA dopaminergic circuit and its mesocortical and mesolimbic branches have however complex afferent and efferent pathways that operate in multiple feedback loops [ 35 ]. Cabib and Puglisi-Allegra [ 16 ] have built a compelling case that enhanced tonic mesoaccumbens dopamine activity supports the expression of active stress-induced coping styles, while inhibition of dopamine release is required for passive coping (immobility) in the FST.…”

Section: Forced Swimmentioning

confidence: 99%

Coping with the Forced Swim Stressor: Towards Understanding an Adaptive Mechanism

2016

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In the forced swim test (FST) rodents progressively show increased episodes of immobility if immersed in a beaker with water from where escape is not possible. In this test, a compound qualifies as a potential antidepressant if it prevents or delays the transition to this passive (energy conserving) behavioural style. In the past decade however the switch from active to passive “coping” was used increasingly to describe the phenotype of an animal that has been exposed to a stressful history and/or genetic modification. A PubMed analysis revealed that in a rapidly increasing number of papers (currently more than 2,000) stress-related immobility in the FST is labeled as a depression-like phenotype. In this contribution we will examine the different phases of information processing during coping with the forced swim stressor. For this purpose we focus on the action of corticosterone that is mediated by the closely related mineralocorticoid receptors (MR) and glucocorticoid receptors (GR) in the limbic brain. The evidence available suggests a model in which we propose that the limbic MR-mediated response selection operates in complementary fashion with dopaminergic accumbens/prefrontal executive functions to regulate the transition between active and passive coping styles. Upon rescue from the beaker the preferred, mostly passive, coping style is stored in the memory via a GR-dependent action in the hippocampal dentate gyrus. It is concluded that the rodent's behavioural response to a forced swim stressor does not reflect depression. Rather the forced swim experience provides a unique paradigm to investigate the mechanistic underpinning of stress coping and adaptation.

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“…Nicotine is well‐known for its regulatory actions on the reward system. Nicotine exerts its effects through nicotinic receptors expressed in the VTA, striatum, and PFC (de Kloet, Mansvelder, & De Vries, ). Studies indicate that endogenous opioids have a role in the rewarding effects of nicotine (Noble, Lenoir, & Marie, ).…”

Section: Introductionmentioning

confidence: 99%

Chronic nicotine-induced changes in gene expression of delta and kappa-opioid receptors and their endogenous ligands in the mesocorticolimbic system of the rat

Ugur

Kaya

Gozen

et al. 2017

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Delta and kappa opioid receptors (DOR and KOR, respectively) and their endogenous ligands, proenkephalin (PENK) and prodynorphin (PDYN)-derived opioid peptides are proposed as important mediators of nicotine reward. This study investigated the regulatory effect of chronic nicotine treatment on the gene expression of DOR, KOR, PENK and PDYN in the mesocorticolimbic system. Three groups of rats were injected subcutaneously with nicotine at doses of 0.2, 0.4, or 0.6 mg/kg/day for 6 days. Rats were decapitated 1 hr after the last dose on day six, as this timing coincides with increased dopamine release in the mesocorticolimbic system. mRNA levels in the ventral tegmental area (VTA), lateral hypothalamic area (LHA), amygdala (AMG), dorsal striatum (DST), nucleus accumbens, and medial prefrontal cortex were measured by quantitative real-time PCR. Our results showed that nicotine upregulated DOR mRNA in the VTA at all of the doses employed, in the AMG at the 0.4 and 0.6 mg/kg doses, and in the DST at the 0.4 mg/kg dose. Conversely, PDYN mRNA was reduced in the LHA with 0.6 mg/kg nicotine and in the AMG with 0.4 mg/kg nicotine. KOR mRNA was also decreased in the DST with 0.6 mg/kg nicotine. Nicotine did not regulate PENK mRNA in any brain region studied.

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Cholinergic modulation of dopamine pathways through nicotinic acetylcholine receptors

Cited by 56 publications

References 229 publications

The association between the nicotinic acetylcholine receptor α4 subunit gene (CHRNA4) rs1044396 and Internet gaming disorder in Korean male adults

The association between the nicotinic acetylcholine receptor α4 subunit gene (CHRNA4) rs1044396 and Internet gaming disorder in Korean male adults

Coping with the Forced Swim Stressor: Towards Understanding an Adaptive Mechanism

Chronic nicotine-induced changes in gene expression of delta and kappa-opioid receptors and their endogenous ligands in the mesocorticolimbic system of the rat

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