Nicotine Administration Attenuates Methamphetamine-Induced Novel Object Recognition Deficits

Vieira-Brock, Paula L.; McFadden, Lisa M.; Nielsen, Shannon M.; Smith, Michael L.; Hanson, Glen R.; Fleckenstein, Annette E.

doi:10.1093/ijnp/pyv073

Cited by 16 publications

(10 citation statements)

References 74 publications

(127 reference statements)

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“…To examine hippocampus-independent object memory, the mice were subjected to a novel object recognition test after 19–20 weeks of running. This test was conducted in an open field arena (30 cm × 30 cm) as described previously [42]. Both training and trial session duration was 5 min.…”

Section: Methodsmentioning

confidence: 99%

Midlife physical activity is associated with lower incidence of vascular dementia but not Alzheimer’s disease

et al. 2019

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Background Physical activity might reduce the risk of developing dementia. However, it is still unclear whether the protective effect differs depending on the subtype of dementia. We aimed to investigate if midlife physical activity affects the development of vascular dementia (VaD) and Alzheimer’s disease (AD) differently in two large study populations with different designs. Methods Using a prospective observational design, we studied whether long-distance skiers of the Swedish Vasaloppet (n = 197,685) exhibited reduced incidence of VaD or AD compared to matched individuals from the general population (n = 197,684) during 21 years of follow-up (median 10, interquartile range (IQR) 5–15 years). Next, we studied the association between self-reported physical activity, stated twice 5 years apart, and incident VaD and AD in 20,639 participants in the Swedish population-based Malmo Diet and Cancer Study during 18 years of follow-up (median 15, IQR 14–17 years). Finally, we used a mouse model of AD and studied brain levels of amyloid-β, synaptic proteins, and cognitive function following 6 months of voluntary wheel running. Results Vasaloppet skiers (median age 36.0 years [IQR 29.0–46.0], 38% women) had lower incidence of all-cause dementia (adjusted hazard ratio (HR) 0.63, 95% CI 0.52–0.75) and VaD (adjusted HR 0.49, 95% CI 0.33–0.73), but not AD, compared to non-skiers. Further, faster skiers exhibited a reduced incidence of VaD (adjusted HR 0.38, 95% CI 0.16–0.95), but not AD or all-cause dementia compared to slower skiers. In the Malmo Diet and Cancer Study (median age 57.5 years [IQR 51.0–63.8], 60% women), higher physical activity was associated with reduced incidence of VaD (adjusted HR 0.65, 95% CI 0.49-0.87), but not AD nor all-cause dementia. These findings were also independent of APOE-ε4 genotype. In AD mice, voluntary running did not improve memory, amyloid-β, or synaptic proteins. Conclusions Our results indicate that physical activity in midlife is associated with lower incidence of VaD. Using three different study designs, we found no significant association between physical activity and subsequent development of AD.

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Section: Methodsmentioning

confidence: 99%

Midlife physical activity is associated with lower incidence of vascular dementia but not Alzheimer’s disease

et al. 2019

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“…Eight slices (four per rat) were mounted on each Superfrost Plus glass microslide (VWR International, Radnor, PA) and stored at 280°C for subsequent use in autoradiography assays. Hippocampal and perirhinal cortex tissues were also analyzed and data were reported in a separate article (Vieira-Brock et al, 2015).…”

Section: Methodsmentioning

confidence: 99%

Chronic Nicotine Exposure Attenuates Methamphetamine-Induced Dopaminergic Deficits

Vieira-Brock

McFadden

Nielsen

et al. 2015

J Pharmacol Exp Ther

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Repeated methamphetamine (METH) administrations cause persistent dopaminergic deficits resembling aspects of Parkinson's disease. Many METH abusers smoke cigarettes and thus selfadminister nicotine; yet few studies have investigated the effects of nicotine on METH-induced dopaminergic deficits. This interaction is of interest because preclinical studies demonstrate that nicotine can be neuroprotective, perhaps owing to effects involving a4b2 and a6b2 nicotinic acetylcholine receptors (nAChRs). This study revealed that oral nicotine exposure beginning in adolescence [postnatal day (PND) 40] through adulthood [PND 96] attenuated METH-induced striatal dopaminergic deficits when METH was administered at PND 89. This protection did not appear to be due to nicotine-induced alterations in METH pharmacokinetics. Short-term (i.e., 21-day) high-dose nicotine exposure also protected when administered from PND 40 to PND 61 (with METH at PND 54), but this protective effect did not persist. Short-term (i.e., 21-day) high-dose nicotine exposure did not protect when administered postadolescence (i.e., beginning at PND 61, with METH at PND 75). However, protection was engendered if the duration of nicotine exposure was extended to 39 days (with METH at PND 93). Autoradiographic analysis revealed that nicotine increased striatal a4b2 expression, as assessed using [125 I]epibatidine. Both METH and nicotine decreased striatal a6b2 expression, as assessed using [125 I]aconotoxin MII. These findings indicate that nicotine protects against METH-induced striatal dopaminergic deficits, perhaps by affecting a4b2 and/or a6b2 expression, and that both age of onset and duration of nicotine exposure affect this protection.

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“…Results from preclinical studies also suggest that nicotine may alleviate some of the adverse consequences of chronic stimulant use. A recent series of studies found that nicotine exposure attenuated METH-induced disruptions in cognitive performance and striatal deficits possibly through activation of α4β2 receptors [122–124]. Nicotine and other nAChR agonists have also been shown to ameliorate disruptions in cognitive performance in monkeys with a history of cocaine self-administration [125].…”

Section: Nicotine + Stimulant Interactionsmentioning

confidence: 99%

Interactions between nicotine and drugs of abuse: a review of preclinical findings

Kohut

2016

The American Journal of Drug and Alcohol Abuse

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Polysubstance abuse is common among substance use disorder patients and nicotine is one of the most commonly co-used substances. Epidemiological and clinical laboratory studies suggest that nicotine, when combined with other drugs of abuse, increases intake of one or both substances. This review focuses on the preclinical literature regarding nicotine’s interaction with alcohol, stimulants (i.e., cocaine, amphetamines), opioids (i.e., morphine, heroin) and Δ9-tetrahydrocannabinol (THC). The current understanding of how these various classes of abused drugs may interact with nicotine on behavioral, physiological, and pharmacological indices that may be important in maintaining co-use of one or both substances in human populations are highlighted. Suggestions as to future areas of research and gaps in knowledge are offered.

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Nicotine Administration Attenuates Methamphetamine-Induced Novel Object Recognition Deficits

Cited by 16 publications

References 74 publications

Midlife physical activity is associated with lower incidence of vascular dementia but not Alzheimer’s disease

Midlife physical activity is associated with lower incidence of vascular dementia but not Alzheimer’s disease

Chronic Nicotine Exposure Attenuates Methamphetamine-Induced Dopaminergic Deficits

Interactions between nicotine and drugs of abuse: a review of preclinical findings

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