Nicotinic Receptors

2014

DOI: 10.1007/978-1-4939-1167-7_18

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Nicotinic Acetylcholine Receptors Along the Habenulo-Interpeduncular Pathway: Roles in Nicotine Withdrawal and Other Aversive Aspects

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Mariella De Biasi

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Cited by 3 publications

References 169 publications

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Healthy Smoker: An Oxymoron? Maybe, But It Is More Complicated Than That

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et al. 2018

Putting Systems and Complexity Sciences Into Practice

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Healthy Smoker: An Oxymoron? Maybe, But It Is More Complicated Than That

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,

²

,

³

et al. 2018

Putting Systems and Complexity Sciences Into Practice

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α2-Null mutant mice have altered levels of neuronal activity in restricted midbrain and limbic brain regions during nicotine withdrawal as demonstrated by cfos expression

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2015

Biochemical Pharmacology

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Neuronal nicotinic acetylcholine receptors (nAChRs) are the primary binding sites for nicotine within the brain. Using alpha(α)2 nAChR subunit-null mutant mice, the current study evaluates whether the absence of this gene product during mecamylamine-precipitated nicotine withdrawal eliminates neuronal activity within selective midbrain and limbic brain regions, as determined by the expression of the immediate early gene, cfos. Our results demonstrate that nicotine withdrawal enhances neuronal activity within the interpeduncular nucleus and dorsal hippocampus, which is absent in mice null for α2-containing nAChRs. In contrast, we observe that α2-null mutant mice exhibit a suppression of neuronal activity in the dentate gyrus in mice undergoing nicotine withdrawal. Interestingly, α2-null mutant mice display potentiated neuronal activity specifically within the stratum lacunosum moleculare layer of the hippocampus, independent of nicotine withdrawal. Overall, our findings demonstrate that α2-null mutant mice have altered cfos expression in distinct populations of neurons within selective midbrain and limbic brain structures that mediate baseline and nicotine withdrawal-induced neuronal activity.

Smokers Display Reduced Glucocorticoid Sensitivity Prior to Symptomatic Chronic Disease Development

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et al. 2018

Annals of Behavioral Medicine

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Cigarette smoking, a self-initiated pharmacological chronic stressor, may provide a unique opportunity to examine early wear and tear on physiological functioning that may lead to chronic disease development. Additional research into PBMCs' intracellular changes must be examined as well as repeating this study in a larger, more heterogeneous population.

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