Nicotinic Acetylcholine Receptor-Mediated [<sup>3</sup>H]Dopamine Release from Hippocampus

Cao, Ying-Jun; Surowy, Carol S.; Puttfarcken, Pamela S.

doi:10.1124/jpet.104.076794

Cited by 29 publications

(12 citation statements)

References 36 publications

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“…However, it cannot be ruled out that the MLA concentration used in this study failed to antagonize nicotine's effects. On the other hand, studies have shown that a7 homomeric receptors play only a minor role in nicotine-mediated presynaptic catecholamine release (Matta et al, 1995;Cao et al, 2005) and that neuronal activity in hypothalamic neurons is unaffected by an a7-selective antagonist , indicating that a7 would not regulate weight through either presynaptic or postsynaptic mechanisms. Thus, evidence points to heteromeric nAChRs to mediate the anorexic properties of nicotine in developing animals.…”

Section: Mechanisms Of Nicotine-induced Growth Retardationmentioning

confidence: 95%

Chronic nicotine induces growth retardation in neonatal rat pups

et al. 2006

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Section: Mechanisms Of Nicotine-induced Growth Retardationmentioning

confidence: 95%

Chronic nicotine induces growth retardation in neonatal rat pups

et al. 2006

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“…also indirectly modulate dopamine release in the prefrontal cortex and fine tune dopamine neuron firing in the ventral tegmental area (Mameli-Engvall et al 2006;Livingstone et al 2009). In contrast, α3β4 nAChRs are expressed predominantly in the medial habenula and interpeduncular nucleus, stimulating both acetylcholine and glutamate release in these nuclei (Perry et al 2002;Grady et al 2009;Fowler et al 2011), as well as dopamine release in the hippocampus (Cao et al 2005).…”

Section: Microcircuitry Of the Nucleus Accumbens (Nac) Showing Devementioning

confidence: 99%

Nicotine and the adolescent brain

Yuan¹,

Cross

Loughlin³

et al. 2015

The Journal of Physiology

402

294

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Adolescence encompasses a sensitive developmental period of enhanced clinical vulnerability to nicotine, tobacco, and e-cigarettes. While there are sociocultural influences, data at preclinical and clinical levels indicate that this adolescent sensitivity has strong neurobiological underpinnings. Although definitions of adolescence vary, the hallmark of this period is a profound reorganization of brain regions necessary for mature cognitive and executive function, working memory, reward processing, emotional regulation, and motivated behavior. Regulating critical facets of brain maturation are nicotinic acetylcholine receptors (nAChRs). However, perturbations of cholinergic systems during this time with nicotine, via tobacco or e-cigarettes, have unique consequences on adolescent development. In this review, we highlight recent clinical and preclinical data examining the adolescent brain's distinct neurobiology and unique sensitivity to nicotine. First, we discuss what defines adolescence before reviewing normative structural and neurochemical alterations that persist until early adulthood, with an emphasis on dopaminergic systems. We review how acute exposure to nicotine impacts brain development and how drug responses differ from those seen in adults. Finally, we discuss the persistent alterations in neuronal signaling and cognitive function that result from chronic nicotine exposure, while highlighting a low dose, semi-chronic exposure paradigm that may better model adolescent tobacco use. We argue that nicotine exposure, increasingly occurring as a result of e-cigarette use, may induce epigenetic changes that sensitize the brain to other drugs and prime it for future substance abuse.

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“…Stimulation of D2 receptors with quinpirole increases DA clearance in in vivo voltammetry studies and increases DA uptake in in vitro studies [71, 73], whereas inhibition of D2 receptors by raclopride decreases DA clearance in voltammetry studies [72]. Nicotine increased DA release in mPFC [170, 289, 290], and increases in extracellular DA concentrations would be expected to stimulate D2 receptors, which could then augment DAT function indirectly. It remains to be determined if nicotine differentially augments DA release in mPFC in EC and IC, which could result in differential stimulation of D2 receptors in the mPFC or if enrichment alters mPFC D2 receptor function.…”

Section: Individual Differences In Dat Function In Response To Psymentioning

confidence: 99%

Role of the Dopamine Transporter in the Action of Psychostimulants, Nicotine, and Other Drugs of Abuse

Zhu

Reith²

2008

CNSNDDT

119

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A number of studies over the last two decades have demonstrated the critical importance of dopamine (DA) in the behavioral pharmacology and addictive properties of abused drugs. The DA transporter (DAT) is a major target for drugs of abuse in the category of psychostimulants, and for methylphenidate (MPH), a drug used for treating attention deficit hyperactivity disorder (ADHD), which can also be a psychostimulant drug of abuse. Other drugs of abuse such as nicotine, ethanol, heroin and morphine interact with the DAT in more indirect ways. Despite the different ways in which drugs of abuse can affect DAT function, one evolving theme in all cases is regulation of the DAT at the level of surface expression. DAT function is dynamically regulated by multiple intracellular and extracellular signaling pathways and several protein-protein interactions. In addition, DAT expression is regulated through the removal (internalization) and recycling of the protein from the cell surface. Furthermore, recent studies have demonstrated that individual differences in response to novel environments and psychostimulants can be predicted based on individual basal functional DAT expression. Although current knowledge of multiple factors regulating DAT activity has greatly expanded, many aspects of this regulation remain to be elucidated; these data will enable efforts to identify drugs that might be used therapeutically for drug dependence therapeutics.

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Nicotinic Acetylcholine Receptor-Mediated [³H]Dopamine Release from Hippocampus

Cited by 29 publications

References 36 publications

Chronic nicotine induces growth retardation in neonatal rat pups

Chronic nicotine induces growth retardation in neonatal rat pups

Nicotine and the adolescent brain

Role of the Dopamine Transporter in the Action of Psychostimulants, Nicotine, and Other Drugs of Abuse

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Nicotinic Acetylcholine Receptor-Mediated [3H]Dopamine Release from Hippocampus

Cited by 29 publications

References 36 publications

Chronic nicotine induces growth retardation in neonatal rat pups

Chronic nicotine induces growth retardation in neonatal rat pups

Nicotine and the adolescent brain

Role of the Dopamine Transporter in the Action of Psychostimulants, Nicotine, and Other Drugs of Abuse

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Product

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Nicotinic Acetylcholine Receptor-Mediated [³H]Dopamine Release from Hippocampus