Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 3 complete abstracts (653 words), 9 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
A nicotinic antagonist that is well absorbed from the gastrointestinal tract and crosses the blood-brain barrier. Mecamylamine has been used as a ganglionic blocker in treating hypertension, but, like most ganglionic blockers, is more often used now as a research tool.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Where it fits in the MeSH classification
- Broader topics
- Norbornanes
Research landscape
PubMed indexes 1,998 records tagged with the MeSH heading “Mecamylamine” (counts retrieved 2026-10-31). 73 of them (3.7%) were published from 2020 onward, and the busiest period so far is through 1999 with 1,034 records.
Reviews account for 38 records (1.9%) and meta-analyses for 0. Randomized controlled trials number 41 (2.1%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 1,034 |
| 2000-2009 | 530 |
| 2010-2019 | 361 |
| 2020 onward | 73 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 38 | 1.9% |
| Meta-analyses | 0 | 0.0% |
| Randomized controlled trials | 41 | 2.1% |
Method: PubMed query "Mecamylamine"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-31.
Reading the evidence in drugs and chemicals
Studies of a chemical or drug can answer very different questions: what it is and how it behaves in cells and animals, how the body handles it, and whether it changes outcomes in people. Laboratory and animal findings often do not carry over to patients, and observational studies of exposures are confounded by who uses a substance and why. Nothing on this page is a recommendation to use, avoid, start or stop any substance or medicine; talk to a qualified clinician or pharmacist about your own situation. Check the dose, the species, the comparison group and whether a patient-relevant outcome was measured.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Gestational exposure of mice to secondhand cigarette smoke causes bronchopulmonary dysplasia blocked by the nicotinic receptor antagonist mecamylamine | 2013 | Research article Design not recorded in structured metadata | 26 | cc0 PMID 23757602 · DOI · PMC3734504 |
| Inhibiting cholinergic signalling in the cerebellar interpositus nucleus impairs motor behaviour | 2024 | Research article Design not recorded in structured metadata | 5 | cc by PMID 37455360 · DOI · PMC7616440 |
| Mecamylamine inhibits seizure-like activity in CA1-CA3 hippocampus through antagonism to nicotinic receptors | 2021 | Research article Design not recorded in structured metadata | 2 | cc by PMID 33711021 · DOI · PMC7954330 |
Gestational exposure of mice to secondhand cigarette smoke causes bronchopulmonary dysplasia blocked by the nicotinic receptor antagonist mecamylamine [1]
Abstract reading summary — source excerpts
- Opening excerpt
- BackgroundCigarette smoke (CS) exposure during gestation may increase the risk of bronchopulmonary dysplasia (BPD)-a developmental lung condition primarily seen in neonates that is characterized by hypoalveolarization, decreased angiogenesis, and diminished surfactant protein production and may increase the risk of chronic obstructive pulmonary disease.
- Closing excerpt
- Nicotinic receptors are critical in the induction of gestational SS-induced BPD, and the use of nAChR antagonists during pregnancy may block CS-induced BPD.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (215 words)
BackgroundCigarette smoke (CS) exposure during gestation may increase the risk of bronchopulmonary dysplasia (BPD)-a developmental lung condition primarily seen in neonates that is characterized by hypoalveolarization, decreased angiogenesis, and diminished surfactant protein production and may increase the risk of chronic obstructive pulmonary disease.ObjectiveWe investigated whether gestational exposure to secondhand CS (SS) induced BPD and sought to ascertain the role of nicotinic acetylcholine receptors (nAChRs) in this response.MethodsWe exposed BALB/c and C57BL/6 mice to filtered air (control) or SS throughout the gestation period or postnatally up to 10 weeks. Lungs were examined at 7 days, 10 weeks, and 8 months after birth.ResultsGestational but not postnatal exposure to SS caused a typical BPD-like condition: suppressed angiogenesis [decreased vascular endothelial growth factor (VEGF), VEGF receptor, and CD34/CD31 (hematopoietic progenitor cell marker/endothelial cell marker)], irreversible hypoalveolarization, and significantly decreased levels of Clara cells, Clara cell secretory protein, and surfactant proteins B and C, without affecting airway ciliated cells. Importantly, concomitant exposure to SS and the nAChR antagonist mecamylamine during gestation blocked the development of BPD.ConclusionsGestational exposure to SS irreversibly disrupts lung development leading to a BPD-like condition with hypoalveolarization, decreased angiogenesis, and diminished lung secretory function. Nicotinic receptors are critical in the induction of gestational SS-induced BPD, and the use of nAChR antagonists during pregnancy may block CS-induced BPD.
Abstract reproduced from the open-access article under the recorded cc0 licence; © the authors. PMID 23757602 · DOI · PMC3734504
Inhibiting cholinergic signalling in the cerebellar interpositus nucleus impairs motor behaviour [2]
Abstract reading summary — source excerpts
- Opening excerpt
- The role of neuromodulators in the cerebellum is not well understood.
- Closing excerpt
- Together, these data suggest that acetylcholine in the cerebellar interpositus nucleus is important for the execution and coordination of voluntary movements mainly via muscarinic receptor signalling, especially in relation to reward-related behaviour.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (238 words)
The role of neuromodulators in the cerebellum is not well understood. In particular, the behavioural significance of the cholinergic system in the cerebellum is unknown. To investigate the importance of cerebellar cholinergic signalling in behaviour, we infused acetylcholine receptor antagonists, scopolamine and mecamylamine, bilaterally into the rat cerebellum (centred on interpositus nucleus) and observed the motor effects through a battery of behavioural tests. These tests included unrewarded behaviour during open field exploration and a horizontal ladder walking task and reward-based beam walking and pellet reaching tasks. Infusion of a mix of the antagonists did not impair motor learning in the horizontal ladder walking or the reaching task but reduced spontaneous movement during open field exploration, impaired coordination during beam walking and ladder walking, led to fewer reaches in the pellet reaching task, slowed goal-directed reaching behaviour and reduced reward pellet consumption in a free access to food task. Infusion of the muscarinic antagonist scopolamine on its own resulted in deficits in motor performance and a reduction in the number of reward pellets consumed in the free access to food task. By contrast, infusion of the nicotinic antagonist mecamylamine on its own had no significant effect on any task, except beam walking traversal time, which was reduced. Together, these data suggest that acetylcholine in the cerebellar interpositus nucleus is important for the execution and coordination of voluntary movements mainly via muscarinic receptor signalling, especially in relation to reward-related behaviour.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 37455360 · DOI · PMC7616440
Mecamylamine inhibits seizure-like activity in CA1-CA3 hippocampus through antagonism to nicotinic receptors [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Cholinergic modulation of hippocampal network function is implicated in multiple behavioral and cognitive states.
- Closing excerpt
- The ability of mecamylamine to decrease hippocampal network synchronization might be associated with its therapeutic effects in a wide variety of CNS disorders including addiction, depression and anxiety.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (200 words)
Cholinergic modulation of hippocampal network function is implicated in multiple behavioral and cognitive states. Activation of nicotinic and muscarinic acetylcholine receptors affects neuronal excitability, synaptic transmission and rhythmic oscillations in the hippocampus. In this work, we studied the ability of the cholinergic system to sustain hippocampal epileptiform activity independently from glutamate and GABA transmission. Simultaneous CA3 and CA1 field potential recordings were obtained during the perfusion of hippocampal slices with the aCSF containing AMPA, NMDA and GABA receptor antagonists. Under these conditions, spontaneous epileptiform discharges synchronous between CA3 and CA1 were recorded. Epileptiform discharges were blocked by addition of the calcium-channel blocker Cd2+ and disappeared in CA1 after a surgical cut between CA3 and CA1. Cholinergic antagonist mecamylamine abolished CA3-CA1 synchronous epileptiform discharges, while antagonists of α7 and α4β2 nAChRs, MLA and DhβE, had no effect. Our results suggest that activation of nicotinic acetylcholine receptors can sustain CA3-CA1 synchronous epileptiform activity independently from AMPA, NMDA and GABA transmission. In addition, mecamylamine, but not α7 and α4β2 nAChRs antagonists, reduced bicuculline-induced seizure-like activity. The ability of mecamylamine to decrease hippocampal network synchronization might be associated with its therapeutic effects in a wide variety of CNS disorders including addiction, depression and anxiety.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 33711021 · DOI · PMC7954330
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Mecamylamine - a nicotinic acetylcholine receptor antagonist with potential for the treatment of neuropsychiatric disorders [4]
- Research article Mecamylamine: new therapeutic uses and toxicity/risk profile [5]
- Research article What is the nature of mecamylamine's antagonism of the central effects of nicotine? [6]
- Research article TC-5214 (S-(+)-mecamylamine): a neuronal nicotinic receptor modulator with antidepressant activity [7]
- Research article Mecamylamine (Inversine): an old antihypertensive with new research directions [8]
- Research article Potential therapeutic uses of mecamylamine and its stereoisomers [9]
References
- Singh SP, Gundavarapu S, Smith KR, Chand HS, Saeed AI, Mishra NC, et al.. Gestational exposure of mice to secondhand cigarette smoke causes bronchopulmonary dysplasia blocked by the nicotinic receptor antagonist mecamylamine. . 2013. PMID 23757602 · DOI · PMC3734504
- Pickford J, Iosif CI, Bashir ZI, Apps R. Inhibiting cholinergic signalling in the cerebellar interpositus nucleus impairs motor behaviour. . 2024. PMID 37455360 · DOI · PMC7616440
- Zapukhliak O, Netsyk O, Romanov A, Maximyuk O, Oz M, Holmes GL, et al.. Mecamylamine inhibits seizure-like activity in CA1-CA3 hippocampus through antagonism to nicotinic receptors. . 2021. PMID 33711021 · DOI · PMC7954330
- Bacher I, Wu B, Shytle DR, George TP. Mecamylamine - a nicotinic acetylcholine receptor antagonist with potential for the treatment of neuropsychiatric disorders. Expert Opin Pharmacother. 2009. PMID 19874251 · DOI
- Young JM, Shytle RD, Sanberg PR, George TP. Mecamylamine: new therapeutic uses and toxicity/risk profile. Clin Ther. 2001. PMID 11354389 · DOI
- Martin BR, Onaivi ES, Martin TJ. What is the nature of mecamylamine's antagonism of the central effects of nicotine?. Biochem Pharmacol. 1989. PMID 2684166 · DOI
- Lippiello PM, Beaver JS, Gatto GJ, James JW, Jordan KG, Traina VM, et al.. TC-5214 (S-(+)-mecamylamine): a neuronal nicotinic receptor modulator with antidepressant activity. CNS Neurosci Ther. 2008. PMID 19040552 · DOI · PMC6494058
- Shytle RD, Penny E, Silver AA, Goldman J, Sanberg PR. Mecamylamine (Inversine): an old antihypertensive with new research directions. J Hum Hypertens. 2002. PMID 12080428 · DOI
- Nickell JR, Grinevich VP, Siripurapu KB, Smith AM, Dwoskin LP. Potential therapeutic uses of mecamylamine and its stereoisomers. Pharmacol Biochem Behav. 2013. PMID 23603417 · DOI · PMC3690754
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-31.
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Evidence strength
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