Editing Nicotine (section)

==Research==
===Central nervous system===
While acute/initial nicotine intake causes activation of neuronal nicotinic receptors, chronic low doses of nicotine use leads to desensitization of those receptors (due to the development of tolerance) and results in an antidepressant effect, with early research showing low dose nicotine patches could be an effective treatment of [[major depressive disorder]] in non-smokers.<ref name="pmid20965579">{{cite journal | vauthors = Mineur YS, Picciotto MR | title = Nicotine receptors and depression: revisiting and revising the cholinergic hypothesis | journal = Trends in Pharmacological Sciences | volume = 31 | issue = 12 | pages = 580–6 | date = December 2010 | pmid = 20965579 | pmc = 2991594 | doi = 10.1016/j.tips.2010.09.004 }}</ref>

Though tobacco smoking is associated with an increased risk of [[Alzheimer's disease]],<ref name="pmid19105840">{{cite journal | vauthors = Peters R, Poulter R, Warner J, Beckett N, Burch L, Bulpitt C | title = Smoking, dementia and cognitive decline in the elderly, a systematic review | journal = BMC Geriatrics | volume = 8 | page = 36 | date = December 2008 | pmid = 19105840 | pmc = 2642819 | doi = 10.1186/1471-2318-8-36 | doi-access = free }}</ref> there is evidence that nicotine itself has the potential to prevent and treat Alzheimer's disease.<ref name=pmid19184661>{{cite book |vauthors=Henningfield JE, Zeller M |volume=192 |issue=192 |pages=511–34 |year=2009 |pmid=19184661 |doi=10.1007/978-3-540-69248-5_18 |isbn=978-3-540-69246-1 |series=Handbook of Experimental Pharmacology |title=Nicotine Psychopharmacology |chapter=Nicotine Psychopharmacology: Policy and Regulatory }}</ref>

Smoking is associated with a decreased risk of [[Parkinson's disease]]; however, it is unknown whether this is due to people with healthier brain dopaminergic reward centers (the area of the brain affected by Parkinson's) being more likely to enjoy smoking and thus pick up the habit, nicotine directly acting as a [[Neuroprotection|neuroprotective agent]], or other compounds in cigarette smoke acting as neuroprotective agents.<ref>{{cite journal | vauthors = Quik M, O'Leary K, Tanner CM | title = Nicotine and Parkinson's disease: implications for therapy | journal = Movement Disorders | volume = 23 | issue = 12 | pages = 1641–52 | date = September 2008 | pmid = 18683238 | pmc = 4430096 | doi = 10.1002/mds.21900 }}</ref>

Nicotine may partly attenuate [[sensory gating]] and attentional deficits associated with [[schizophrenia]]. Short-term use of [[transdermal]] nicotine was found to improve subjects’ reaction time and [[Vigilance (psychology)|alertness]] in given tasks. Nicotine was not found to improve [[Negative symptoms of schizophrenia|negative]], [[Psychosis|positive]], or other cognitive symptoms of schizophrenia.<ref>{{cite journal |vauthors=Harris JG, Kongs S, Allensworth D, Martin L, Tregellas J, Sullivan B, Zerbe G, Freedman R |date=July 2004 |title=Effects of nicotine on cognitive deficits in schizophrenia |journal=Neuropsychopharmacology |volume=29 |issue=7 |pages=1378–1385 |doi=10.1038/sj.npp.1300450 |pmid=15138435}}</ref>

===Immune system===
Immune cells of both the [[innate|innate immune system]] and [[adaptive immune system]]s frequently express the α<sub>2</sub>, α<sub>5</sub>, α<sub>6</sub>, α<sub>7</sub>, α<sub>9</sub>, and α<sub>10</sub> [[Nicotinic acetylcholine receptor#Subunits|subunits of nicotinic acetylcholine receptors]].<ref name=":0">{{cite journal | vauthors = Fujii T, Mashimo M, Moriwaki Y, Misawa H, Ono S, Horiguchi K, Kawashima K | title = Expression and Function of the Cholinergic System in Immune Cells | journal = Frontiers in Immunology | volume = 8 | page = 1085 | date = 2017 | pmid = 28932225 | pmc = 5592202 | doi = 10.3389/fimmu.2017.01085 | doi-access = free }}</ref> Evidence suggests that nicotinic receptors which contain these subunits are involved in the regulation of [[immune function]].<ref name=":0" />

===Optopharmacology===
A [[photoactivatable probes|photoactivatable]] form of nicotine, which releases nicotine when exposed to [[ultraviolet light]] with certain conditions, has been developed for studying nicotinic acetylcholine receptors in brain tissue.<ref name="pmid29578537">{{cite journal | vauthors = Banala S, Arvin MC, Bannon NM, Jin XT, Macklin JJ, Wang Y, Peng C, Zhao G, Marshall JJ, Gee KR, Wokosin DL, Kim VJ, McIntosh JM, Contractor A, Lester HA, Kozorovitskiy Y, Drenan RM, Lavis LD | title = Photoactivatable drugs for nicotinic optopharmacology | journal = Nature Methods | volume = 15 | issue = 5 | pages = 347–350 | date = May 2018 | pmid = 29578537 | pmc = 5923430 | doi = 10.1038/nmeth.4637 }}</ref>

===Oral health===
Several ''in vitro'' studies have investigated the potential effects of nicotine on a range of oral cells. A recent systematic review concluded that nicotine was unlikely to be cytotoxic to oral cells ''in vitro'' in most physiological conditions but further research is needed.<ref>{{cite journal | vauthors = Holliday RS, Campbell J, Preshaw PM | title = Effect of nicotine on human gingival, periodontal ligament and oral epithelial cells. A systematic review of the literature | journal = Journal of Dentistry | volume = 86 | pages = 81–88 | date = July 2019 | pmid = 31136818 | doi = 10.1016/j.jdent.2019.05.030 | s2cid = 169035502 }}</ref> Understanding the potential role of nicotine in oral health has become increasingly important given the recent introduction of novel nicotine products and their potential role in helping smokers quit.<ref>{{cite journal | vauthors = Holliday R, Preshaw PM, Ryan V, Sniehotta FF, McDonald S, Bauld L, McColl E | title = A feasibility study with embedded pilot randomised controlled trial and process evaluation of electronic cigarettes for smoking cessation in patients with periodontitis | journal = Pilot and Feasibility Studies | volume = 5 | issue = 1 | page = 74 | date = 2019-06-04 | pmid = 31171977 | pmc = 6547559 | doi = 10.1186/s40814-019-0451-4 | doi-access = free }}</ref>