Chronic Nicotine Exposure Attenuates Methamphetamine-Induced Dopaminergic Deficits

Vieira-Brock, Paula L.; McFadden, Lisa M.; Nielsen, Shannon M.; Ellis, Jonathan D.; Walters, Elliot T.; Stout, Kristen A.; McIntosh, J. Michael; Wilkins, Diana G.; Hanson, Glen R.; Fleckenstein, Annette E.

doi:10.1124/jpet.114.221945

Cited by 9 publications

(6 citation statements)

References 66 publications

(77 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Lastly, the current findings add to the growing body of literature suggesting that chronic nicotine treatment (i.e. administered across days) attenuates subsequent methamphetamine-induced dopaminergic deficits (Vieira-Brock et al, 2015). Although it has also been demonstrated that multiple, acute injections (i.e.…”

Section: Discussionsupporting

confidence: 56%

“…Slides were then incubated for 2 h in buffer-sucrose containing 25 pM 125 I-RTI-55 (2200 Ci/mmol, PerkinElmer, Watham, MA). In a previous study conducted in the same laboratory, nonspecific binding was demonstrated by slides incubated in buffer-sucrose containing 25 pM 125 I-RTI-55, 100 nM fluoxetine, and 100 μM nomifensine (Vieira-Brock et al, 2015). Slides were rinsed twice in ice-cold buffer and distilled water for 2 min and air-dried.…”

Section: Methodsmentioning

confidence: 99%

“…Slides were then incubated for 40 min in binding buffer containing 0.015 nM 125 I-epibatidine (2200 Ci/mmol, PerkinElmer, Watham, MA) in the presence of 100 nM αCtxMII. In a previous study conducted in the same laboratory, nonspecific binding was determined by slides incubated in binding buffer containing 0.015 nM 125 I-epibatidine plus 0.1 mM nicotine (Vieira-Brock et al, 2015). Slides were rinsed twice in ice-cold buffer for 5 min followed by a 10 s rinse in distilled water and air-dried.…”

Section: Methodsmentioning

confidence: 99%

“…In support of this notion, studies examining the effects of chronic nicotine on dopaminergic deficits induced by neurotoxic agents, including methamphetamine, have suggested an important role for α4β2* and α6β2* nAChRs (Ryan et al, 2001; Huang et al, 2009; Quik et al, 2013; Vieira-Brock et al, 2015). The majority of these studies examined the ability of chronic nicotine to attenuate long-term (i.e.…”

Section: Introductionmentioning

confidence: 97%

“…For instance, clinical findings indicate that there is a decreased incidence of Parkinson's disease among cigarette smokers relative to non-smokers (Chen et al, 2010). In addition, preclinical findings in both rodent and nonhuman primate models demonstrate that nicotine treatment attenuates nigrostriatal damage induced by toxins, including repeated, high-doses of methamphetamine (Ryan et al, 2001; O'Neill et al, 2002; Quik et al, 2007; Picciotto and Zoli, 2008; Vieira-Brock et al, 2015). …”

Section: Introductionmentioning

confidence: 99%

See 4 more Smart Citations

Prior nicotine self-administration attenuates subsequent dopaminergic deficits of methamphetamine in rats: role of nicotinic acetylcholine receptors

Baladi

Nielsen²,

McIntosh³

et al. 2016

Behavioural Pharmacology

Self Cite

View full text Add to dashboard Cite

Preclinical studies have demonstrated that oral nicotine exposure attenuates long-term dopaminergic damage induced by toxins, including repeated, high doses of methamphetamine. It is suggested that alterations in nicotinic acetylcholine receptor (nAChR) expression, including α4β2* and α6β2* subtypes, likely contribute to this protection. The current study extended these findings by investigating whether nicotine self-administration in male, Sprague-Dawley rats 1): attenuates short-term dopaminergic damage induced by methamphetamine and 2) causes alterations in levels of α4β2* and α6β2* nAChR subtypes. The findings indicate that nicotine self-administration (0.032 mg/kg/infusion for 14 days) per se did not alter α4β2* and α6β2* nAChR expression or dopamine transporter (DAT) expression and function. Interestingly, prior nicotine self-administration attenuated methamphetamine-induced decreases in DAT function when assessed 24 h, but not 1 h, after methamphetamine treatment (4 × 7.5 mg/kg/injection). The ability of nicotine to attenuate the effects of methamphetamine on DAT function corresponded with increases in α4β2*, but not α6β2*, nAChR binding density. Understanding the role of nAChRs in methamphetamine-induced damage has the potential to elucidate mechanisms underlying the etiology of disorders involving dopaminergic dysfunction, as well as to highlight potential new therapeutic strategies for prevention or reduction of dopaminergic neurodegeneration.

show abstract

Section: Discussionsupporting

confidence: 56%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 97%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Prior nicotine self-administration attenuates subsequent dopaminergic deficits of methamphetamine in rats: role of nicotinic acetylcholine receptors

Baladi

Nielsen²,

McIntosh³

et al. 2016

Behavioural Pharmacology

Self Cite

View full text Add to dashboard Cite

show abstract

Preclinical Evidence for a Role of the Nicotinic Cholinergic System in Parkinson’s Disease

Perez

2015

Neuropsychol Rev

View full text Add to dashboard Cite

One of the primary deficits in Parkinson's disease (PD) is the loss of dopaminergic neurons in the substantia nigra pars compacta which leads to striatal dopaminergic deficits that underlie the motor symptoms associated with the disease. A plethora of animal models have been developed over the years to uncover the molecular alterations that lead to PD development. These models have provided valuable information on neurotransmitter pathways and mechanisms involved. One such a system is the nicotinic cholinergic system. Numerous studies show that nigrostriatal damage affects nicotinic receptor-mediated dopaminergic signaling; therefore therapeutic modulation of the nicotinic cholinergic system may offer a novel approach to manage PD. In fact, there is evidence showing that nicotinic receptor drugs may be useful as neuroprotective agents to prevent Parkinson's disease progression. Additional preclinical studies also show that nicotinic receptor drugs may be beneficial for the treatment of L-dopa induced dyskinesias. Here, we review preclinical findings supporting the idea that nicotinic receptors are valuable therapeutic targets for PD.

show abstract

Chronic Tobacco-Smoking on Psychopathological Symptoms, Impulsivity and Cognitive Deficits in HIV-Infected Individuals

Chang

Lim

Lau

et al. 2017

J Neuroimmune Pharmacol

View full text Add to dashboard Cite

HIV-infected individuals (HIV+) has 2–3 times the rate of tobacco smoking than the general population, and whether smoking may lead to greater psychiatric symptoms or cognitive deficits remains unclear. We evaluated the independent and combined effects of being HIV+ and chronic tobacco-smoking on impulsivity, psychopathological symptoms and cognition. 104 participants [27 seronegative (SN)-non-Smokers, 26 SN-Smokers, 29 HIV+non-Smokers, 22 HIV+Smokers] were assessed for psychopathology symptoms (Symptom Checklist-90, SCL-90), depressive symptoms (Center for Epidemiologic Studies-Depression Scale, CES-D), impulsivity (Barratt Impulsiveness Scale, BIS), decision-making (The Iowa Gambling Task, IGT, and Wisconsin Card Sorting Test, WCST), and cognition (seven neurocognitive domains). Both HIV+ and Smoker groups had higher SCL-90 and CES-D scores, with highest scores in HIV+Smokers. On BIS, both HIV+ and Smokers had higher Total Impulsiveness scores, with higher behavioral impulsivity in Smokers, highest in HIV+Smokers. Furthermore, across the four groups, HIV+Smokers lost most money and made fewest advantageous choices on the IGT, and had highest percent errors on WCST. Lastly, HIV+ had lower z-scores on all cognitive domains, with the lowest scores in HIV+Smokers. These findings suggest that HIV-infection and chronic tobacco smoking may lead to additive deleterious effects on impulsivity, psychopathological (especially depressive) symptoms and cognitive dysfunction. Although greater impulsivity may be premorbid in HIV+ and Smokers, the lack of benefits of nicotine in chronic Smokers on attention and psychopathology, especially those with HIV-infection, may be due to the negative effects of chronic smoking on dopaminergic and cardio-neurovascular systems. Tobacco smoking may contribute to psychopathology and neurocognitive disorders in HIV+ individuals.

show abstract

Chronic Nicotine Exposure Attenuates Methamphetamine-Induced Dopaminergic Deficits

Cited by 9 publications

References 66 publications

Prior nicotine self-administration attenuates subsequent dopaminergic deficits of methamphetamine in rats: role of nicotinic acetylcholine receptors

Prior nicotine self-administration attenuates subsequent dopaminergic deficits of methamphetamine in rats: role of nicotinic acetylcholine receptors

Preclinical Evidence for a Role of the Nicotinic Cholinergic System in Parkinson’s Disease

Chronic Tobacco-Smoking on Psychopathological Symptoms, Impulsivity and Cognitive Deficits in HIV-Infected Individuals

Contact Info

Product

Resources

About