Nicotine activates and desensitizes midbrain dopamine neurons
Abstract
Tobacco use in developed countries is estimated to be the single largest cause of premature death. Nicotine is the primary component of tobacco that drives use, and like other addictive drugs, nicotine reinforces self-administration and place preference in animal studies. Midbrain dopamine neurons normally help to shape behaviour by reinforcing biologically rewarding events, but addictive drugs such as cocaine can inappropriately exert a reinforcing influence by acting upon the mesolimbic dopamine system. Here we show that the same concentration of nicotine achieved by smokers activates and desensitizes multiple nicotinic receptors thereby regulating the activity of mesolimbic dopamine neurons. Initial application of nicotine can increase the activity of the dopamine neurons, which could mediate the rewarding aspects of tobacco use. Prolonged exposure to even these low concentrations of nicotine, however, can cause desensitization of the nicotinic receptors, which helps to explain acute tolerance to nicotine's effects. The effects suggest a cellular basis for reports that the first cigarette of the day is the most pleasurable, whereas the effect of subsequent cigarettes may depend on the interplay between activation and desensitization of multiple nicotinic receptors.
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Steady states of nicotine that would be achieved in the bloodstream of a regular smoker can desensitize midbrain nAChRs with a time course of recovery that requires several minutes.
“In addition, electrophysiological studies show that steady states of nicotine that would be achieved in the bloodstream of a regular smoker can desensitize midbrain nAChRs with a time course of recovery that requires several minutes (Pidoplichko et al., 1997; Wooltorton et al., 2003).”
From It is not “either/or”: Activation and desensitization of nicotinic acetylcholine receptors both contribute to behaviors related to nicotine addiction and mood (2008) · cites this paper as Pidoplichko et al., 1997
At nicotine concentrations of 500 nM or higher, α7* nAChR activation is characterized by fast currents that desensitize on a millisecond timescale while β2* nAChRs desensitize more slowly on a second timescale.
“As mentioned earlier, at nicotine concentrations of 500 nM or higher, electrophysiological studies in combination with pharmacological agents to isolate individual nAChR-mediated currents have shown that α7* nAChR activation is characterized by fast currents that desensitize on a millisecond timescale while β2* nAChRs desensitize more slowly on a second timescale (Couturier et al., 1990a; Giniat”
From It is not “either/or”: Activation and desensitization of nicotinic acetylcholine receptors both contribute to behaviors related to nicotine addiction and mood (2008) · cites this paper as Pidoplichko et al., 1997
Nicotine can directly excite dopaminergic neurons via nicotinic receptors on the somatodendritic region of dopaminergic neurons.
“Nicotine can directly excite dopaminergic neurons via the nicotinic receptors on the somatodendritic region of dopaminergic neurons (Calabresi et al., 1989; Pidoplichko et al., 1997).”
From Dopamine reward circuitry: Two projection systems from the ventral midbrain to the nucleus accumbens–olfactory tubercle complex (2007) · cites this paper as Pidoplichko et al., 1997
These nicotinic receptors appear to be desensitized within a few seconds after exposure to high, reward-mediating concentrations of nicotine.
“However, these receptors appear to be desensitized within a few seconds after exposure to high, reward-mediating concentrations of nicotine (Pidoplichko et al., 1997; 2004; Wooltorton et al., 2003).”
From Dopamine reward circuitry: Two projection systems from the ventral midbrain to the nucleus accumbens–olfactory tubercle complex (2007) · cites this paper as Pidoplichko et al., 1997
Nicotine administration increases extracellular noradrenaline in various parts of the brain.
“Nicotine administration also increases the extracellular noradrenaline in various parts of the brain (32–35);”
From Tobacco addiction (2008) · cites this paper as [33]
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- Authors
- Pidoplichko, V. I., DeBiasi, M., Williams, J. T., & Dani, J. A.
- Affiliations
- Baylor College of Medicine (US)
- Oregon Health & Science University (US)
- Corresponding author
- Dani, John A.
- Venue
- Nature
- Published
- 1997-11
- Volume
- 390
- Issue
- 6658
- Pages
- 401-404
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- OpenAlex
- W1635375164
- Cited by
- 769
- References
- 32
- Citations by year
- 2026: 6 · 2025: 11 · 2024: 6 · 2023: 8 · 2022: 13 · 2021: 10 · 2020: 59 · 2019: 12 · 2018: 17 · 2017: 9 · 2016: 25 · 2015: 16 · 2014: 23 · 2013: 35 · 2012: 28
- FWCI
- 10.92
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nicotinic Acetylcholine Receptors Study
- Health Sciences › Medicine › Physiology › Smoking Behavior and Cessation
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Keywords
- nicotine, nicotinic acetylcholine receptors, receptor desensitization, midbrain dopaminergic neurons, mesolimbic dopamine system, nicotine tolerance, tobacco dependence, drug reinforcement, nicotine self-administration
- MeSH terms
- Acetylcholine, Action Potentials, Animals, Dopamine, Drug Tolerance, Ganglionic Stimulants, Neurons, Nicotine, Nucleus Accumbens, Receptors, Nicotinic, Time Factors, Rats, Sprague-Dawley, Patch-Clamp Techniques, Rats, In Vitro Techniques
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