Nicotine is a parasympathomimetic stimulant found in the nightshade family of plants. The traditional intake is by smoking tobacco, chewing tobacco or through snuff, but today it is possible to consume nicotine without simultaneously being exposed to tobacco. Nicotine can for instance be absorbed from a chewing gum or a transdermal patch. Nicotine absorbed without exposure to tobacco is currently being researched as a potential cognitive enhancer without the drawbacks of tobacco exposure.

Nicotine as a cognition enhancer

Nicotine in tobacco has a long history of being used for its performance-enhancing effects on cognition, alertness and focus. In both human trials and animal trials, nicotine has been showed to temporarily improve visual attention and working memory.

A meta-study1 published in 2010 concluded that nicotine or smoking had significant positive effects on aspects of fine motor abilities, alerting and orienting attention, and episodic and working memory. This meta-study was based on 41 double-blind, placebo-controlled studies.

A continuous low dose of nicotine absorbed from nicotine patches has been shown to be an effective treatment for major depressive disorder, but only in non-smokers.2 (It’s reasonable to assume that being a tobacco chewer, snuff user or similar would also prevent the nicotine patch from having the desired antidepressant effect.)

Jennifer Rusted, professor of experimental psychology at Sussex University, has published a series of studies showing that nicotine increases prospective memory. An increased prospective memory makes it easier to remember and implement a prior intention, e.g. to remember to make that call to the dentist tomorrow just as you planned. The increase is not huge, just around 15 percent in Rusted’s studies.

Nicotine and Alzheimer’s disease

Tobacco smoking is associated with an increased risk of Alzheimer’s, but studies indicate that nicotine in itself may actually be capable of preventing and treating Alzheimer’s disease. For more information, see Henningfield JE, Zeller M (2009). “Nicotine psychopharmacology: policy and regulatory“.  Handbook of Experimental Pharmacology. 192 (192): 511–34.

Short facts about Nicotine

Examples of trade names	Nicorette Nicotrol
Routes of administration	Inhalation Insufflation Oral: buccal Oral: sublingual Oral: ingestion Transdermal Rectal
Pregnancy category	US: D (Evidence of risk)
Formula	C10H14N2

Pharmacodynamics

Central nervous system (CNS)

Nicotine binds to nicotinic acetylcholine receptors in the brain and increases the levels of several neurotransmitters in various brain structures.

A release of dopamine occurs due to nicotine’s ability to activate the cholinergic–dopaminergic reward link in the ventral tegmental area.

Nicotine may also induce the release of endogenous opioids that activate opioid pathways in the reward system.

Sympathetic nervous system

Nicotine activates the sympathetic nervous system, stimulating the release of epinephrine. Epinephrine and norepinephrine are released into the bloodstream. This leads to an increased heart rate, increased blood pressure, increased respiration and increased blood glucose levels.