ArticleNeuropharmacology2012
Low concentrations of nicotine differentially desensitize nicotinic acetylcholine receptors that include α5 or α6 subunits and that mediate synaptosomal neurotransmitter release.
Article in Neuropharmacology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed.
- CHRNA5 gene variation affects the response of VTA dopaminergic neurons during chronic nicotine exposure and withdrawal.Neuropharmacology · 2023Article
- The incentive amplifying effects of nicotine: Roles in alcohol seeking and consumption.Advances in pharmacology (San Diego, Calif.) · 2022Review
- Neurobiological Mechanisms of Nicotine Reward and Aversion.Pharmacological reviews · 2022Review
- Addiction-related neuroadaptations following chronic nicotine exposure.Journal of neurochemistry · 2021Review
- Roles of the Functional Interaction between Brain Cholinergic and Dopaminergic Systems in the Pathogenesis and Treatment of Schizophrenia and Parkinson's Disease.International journal of molecular sciences · 2021Review
- Cholinergic modulation of hierarchical inhibitory control over cortical resting state dynamics: Local circuit modeling of schizophrenia-related hypofrontality.Current research in neurobiology · 2021Article
- Therapeutic potential of α7 nicotinic acetylcholine receptor agonists to combat obesity, diabetes, and inflammation.Reviews in endocrine & metabolic disorders · 2020Review
- Article
- The α5 Nicotinic Acetylcholine Receptor Subunit Differentially Modulates α4β2Frontiers in synaptic neuroscience · 2020Review
- Gene editing vectors for studying nicotinic acetylcholine receptors in cholinergic transmission.The European journal of neuroscience · 2019Article
- Nicotine and alcohol: the role of midbrain dopaminergic neurons in drug reinforcement.The European journal of neuroscience · 2019Review
- The contribution of agonist and antagonist activities of α4β2* nAChR ligands to smoking cessation efficacy: a quantitative analysis of literature data.Psychopharmacology · 2018Review
- TC299423, a Novel Agonist for Nicotinic Acetylcholine Receptors.Frontiers in pharmacology · 2017Article
- Altered nicotine reward-associated behavior following α4 nAChR subunit deletion in ventral midbrain.PloS one · 2017Article
- Postsynaptic nicotinic acetylcholine receptors facilitate excitation of developing CA1 pyramidal neurons.Journal of neurophysiology · 2016Article
- Layer-specific cholinergic control of human and mouse cortical synaptic plasticity.Nature communications · 2016Article
- Comparison of effects produced by nicotine and the α4β2-selective agonist 5-I-A-85380 on intracranial self-stimulation in rats.Experimental and clinical psychopharmacology · 2016Article
- Nicotine Dependence Reveals Distinct Responses from Neurons and Their Resident Nicotinic Receptors in Medial Habenula.Molecular pharmacology · 2015Article
- Nicotine and Resting-State Functional Connectivity: Effects of Intermittent Doses.Nicotine & tobacco research : official journal of the Society for Research on Nicotine and Tobacco · 2015Article
- Anxiolytic-like and anxiogenic-like effects of nicotine are regulated via diverse action at β2*nicotinic acetylcholine receptors.British journal of pharmacology · 2015Article
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
Desensitization is a complex property of nicotinic acetylcholine receptors (nAChR). Several subtypes of nAChR have high sensitivity to nicotine and mediate effects of nicotine at concentrations found in blood of tobacco smokers. Desensitization of some of these receptor subtypes has been studied in model systems, however, other subtypes have been difficult to express heterologously in native forms. In addition, model systems may not have the same accessory molecules and post-translational modifications found in native populations. We have used wild-type and subunit null mutant mice to study desensitization properties of the high sensitivity α4β2-nAChRs including those that have α5 subunits at both GABAergic and dopaminergic nerve terminals. In addition, we have studied the desensitization of one subtype of α6β2-nAChRs at dopaminergic terminals using α4 subunit null mutant mice. Exposure to low nicotine concentrations, leads to rapid, but partial desensitization of activity mediated by these receptors. α4β2-nAChRs including α5 subunits show faster rates of recovery from desensitization than α4β2-nAChRs without α5. Inclusion of the α5 subunit significantly shifts the concentration response for desensitization to higher values, indicating that receptors with α5 subunits are less desensitized by a 10-min exposure to low concentrations of nicotine. Receptors with α6 subunits appear to desensitize to a lesser degree than those with α4 subunits, indicating that α6β2-nAChRs are somewhat resistant to desensitization by nicotine. These results highlight the importance of studying various receptor subtypes in native systems and how they may differentially respond to nicotine and to nicotinic drugs.
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