Nicotine modulates expression of amyloid precursor protein and amyloid precursor-like protein 2 in mouse brain and in SH-SY5Y neuroblastoma cells

Gutala, Ramana; Ju, Wang; Hwang, Young Hwan; Haq, Riaz ul; Li, Ming D.

doi:10.1016/j.brainres.2006.03.100

Cited by 28 publications

(20 citation statements)

References 53 publications

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“…However, nicotine also can interact directly with neuronal cells to regulate some immune-related pathways, and its neuronal protective role has been confirmed by a few independent experts (Kihara et al 1997;Kincade et al 2005). Nicotinic receptors are expressed throughout the nervous system and regulate gene expression in different pathways Lukas 2003, 2006;Gutala et al 2006). Although the neuron has a limited ability to release cytokines and chemokines to evoke the inflammation cascade, nicotine can trigger some immune-related downstream signaling pathways, especially the Ca 2+ -dependent pathways such as phosphatidylinositol 3-kinase (PI3K), protein kinase C (PKC), and CaMKII, getting involved in the regulation of transmitter release, synaptic plasticity, and cell survival and providing benefit in some neuron-degenerative diseases, such as AD and PD (Damaj 2000;Hejmadi et al 2003;Kihara et al 2001;Liu et al 2001;Messing et al 1989;Picciotto and Zoli 2002;Shaw et al 2002).…”

Section: Regulatory Effects Of Nicotine On Neuronsmentioning

confidence: 99%

“…Nicotine can also modulate the expression of numerous genes in neurons (Dunckley and Lukas 2003;Gutala et al 2006). To determine how nicotine regulates multiple immune-related pathways, we treated SH-SY5Y cells, which respond to TLR3 ligand and trigger production of IFN-γ (Zhou et al 2009), with acute nicotine administration, and measured the expression of more than 3,000 genes using microarray technology.…”

Section: Regulatory Effects Of Nicotine On Neuronsmentioning

confidence: 99%

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Nicotinic Modulation of Innate Immune Pathways Via α7 Nicotinic Acetylcholine Receptor

Cui

2010

J Neuroimmune Pharmacol

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The major addictive component of tobacco, nicotine, exerts anti-inflammatory effects in multiple cell types and may benefit neurons in various degenerative disorders, such as Alzheimer's and Parkinson's disease, in which an inflammation-related mechanism is implicated. Among the various nicotinic acetylcholine receptors, α7, which has been identified in both neurons and immune cells and has high permeability to calcium, is believed to contribute significantly to nicotinic anti-inflammatory and neuron-protective effects. Although nicotine has been used in clinical trials for the treatment of some inflammatory diseases such as ulcerative colitis, the molecular mechanisms of its actions are largely unknown. In this review, we provide current evidence for nicotine's modulation of multiple immune pathways via α7 nAChRs in both neurons and immune cells. Understanding the mechanism of the nicotinic anti-inflammatory effect and neuron-protective function may guide the development of novel medicines for infectious and neuron-degenerative diseases.

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Section: Regulatory Effects Of Nicotine On Neuronsmentioning

confidence: 99%

Section: Regulatory Effects Of Nicotine On Neuronsmentioning

confidence: 99%

Nicotinic Modulation of Innate Immune Pathways Via α7 Nicotinic Acetylcholine Receptor

Cui

2010

J Neuroimmune Pharmacol

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“…C57BL/6 mice were chosen because prior reports demonstrate that adult and periadolescent mice from this strain consume nicotine in the concentration used in the present study. In fact, oral nicotine has also been shown to be effective in eliciting behavioral (Adriani et al, 2002(Adriani et al, , 2004Gaddnas et al, 2001) and neurochemical alterations, including nicotinic receptors upregulation (Nuutinen et al, 2005;Sparks and Pauly, 1999), altered monoamine levels, and metabolism (Gaddnas et al, 2000;Tammimaki et al, 2006;Vihavainen et al, 2006) as well as altered expression of genes implicated in synaptic plasticity induced by drugs of abuse (Marttila et al, 2006) and in Alzheimer's disease (Gutala et al, 2006) in this and other mouse strains. This strain of mice is known to present particular features, such as higher voluntary ethanol consumption (Crawley et al, 1997), which should be taken into consideration in studies that involve the administration of this substance, even though the bases underlying these strain-specific characteristics remain poorly understood (Crabbe et al, 1999).…”

Section: Methodological Issuesmentioning

confidence: 87%

Combined Exposure to Nicotine and Ethanol in Adolescent Mice Differentially Affects Anxiety Levels during Exposure, Short-Term, and Long-Term Withdrawal

Abreu‐Villaça

Nunes

Queiroz-Gomes

et al. 2007

Neuropsychopharmacol

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Smoking and consumption of alcoholic beverages are frequently associated during adolescence. This association could be explained by the cumulative behavioral effects of nicotine and ethanol, particularly those related to anxiety levels. However, despite epidemiological findings, there have been few animal studies of the basic neurobiology of the combined exposure in the adolescent brain. In the present work we assessed, through the use of the elevated plus maze, the short-and long-term anxiety effects of nicotine (NIC) and/or ethanol (ETOH) exposure during adolescence (from the 30th to the 45th postnatal day) in four groups of male and female C57BL/6 mice: (1) Concomitant NIC (nicotine free-base solution (50 mg/ml) in 2% saccharin to drink) and ETOH (ethanol solution (25%, 2 g/kg) i.p. injected every other day) exposure; (2) NIC exposure; (3) ETOH exposure; (4) Vehicle. C57BL/6 mice were selected, in spite of the fact that they present slower ethanol metabolism, because they readily consume nicotine in the concentration used in the present study. During exposure (45th postnatal day: PN45), our results indicated that ethanol was anxiolytic in adolescent mice and that nicotine reverted this effect. Short-term drug withdrawal (PN50) elicited sex-dependent effects: exposure to nicotine and/or ethanol was anxiogenic only for females. Although neither nicotine nor ethanol effects persisted up to 1 month postexposure (PN75), the coadministration elicited an anxiogenic response. In spite of the fact that generalizations based on the results from a single strain of mice are prone to shortcomings, our results suggest that the deficient response to the anxiolytic effects of ethanol in adolescents co-exposed to nicotine may drive higher ethanol consumption. Additionally, increased anxiety during long-term smoking and drinking withdrawal may facilitate relapse to drug use.

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“…Some of the effects of this drug are positive, such as neuroprotection against neurotoxic agents, ageing, and pathological situations. [6][7][8][9][10][11][12] Our research group has demonstrated that nicotine increases the turnover of the glycolytic pathway and Krebs cycle in neurons, 13 and the NGF immunoreactivity in the frontoparietal cortex. 14 The benefits of other changes, such as the modification of synaptic transmission 15 and the activation of the midbrain dopamine system, 16 are more debatable.…”

Section: Introductionmentioning

confidence: 99%

FTIR microspectroscopic analysis of the effects of certain drugs on oxidative stress and brain protein structure

et al. 2008

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This study reports the changes in lipids and proteins of different brain areas of nicotine, D(+)‐amphetamine, and nicotine and D(+)‐amphetamine treated rats by monitoring lipid peroxidation and protein β‐sheet formation using infrared microspectroscopy. Compared with the untreated brain samples, the peroxide level is relatively higher in the amphetamine‐treated brain sections, both in the cortex and hippocampus area. However, this peroxide increase is attenuated when administering amphetamine plus nicotine. Analogous drug‐dependent trends for protein β‐sheet content are observed, which suggests a connection between lipid oxidation involved in oxidative stress and β‐sheet protein structure generally present in neurodegenerative diseases. The above property of nicotine is of interest, in the sense that it might reduce the production of β‐amyloid proteins in Alzheimer's disease. © 2008 Wiley Periodicals, Inc. Biopolymers 89: 548–554, 2008.This article was originally published online as an accepted preprint. The (Published Online) date corresponds to the preprint version. You can request a copy of the preprint by emailing the Biopolymers editorial office at biopolymers@wiley.com

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Nicotine modulates expression of amyloid precursor protein and amyloid precursor-like protein 2 in mouse brain and in SH-SY5Y neuroblastoma cells

Cited by 28 publications

References 53 publications

Nicotinic Modulation of Innate Immune Pathways Via α7 Nicotinic Acetylcholine Receptor

Nicotinic Modulation of Innate Immune Pathways Via α7 Nicotinic Acetylcholine Receptor

Combined Exposure to Nicotine and Ethanol in Adolescent Mice Differentially Affects Anxiety Levels during Exposure, Short-Term, and Long-Term Withdrawal

FTIR microspectroscopic analysis of the effects of certain drugs on oxidative stress and brain protein structure

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