Evidence map›Paper›PMID 29549391›Full record

ArticlePsychopharmacology2018

Pharmacological modulation of the α7 nicotinic acetylcholine receptor in a mouse model of mecamylamine-precipitated nicotine withdrawal.

Asti Jackson, Roger L Papke, M Imad Damaj

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Psychopharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.2field-weighted citation impact, top 22% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

11 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Rodent models for nicotine withdrawal.Journal of psychopharmacology (Oxford, England) · 2021
    Review
  6. Review
  7. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 1 country.

Asti JacksonDepartment of Pharmacology and Toxicology, Medical College of Virginia Campus, Virginia Commonwealth University, Richmond, VA, USA. jacksonab2@vcu.edu.
Roger L PapkeDepartment of Pharmacology and Therapeutics, University of Florida, PO Box 100267, Gainesville, FL, 32610-0267, USA.
M Imad DamajDepartment of Pharmacology and Toxicology, Medical College of Virginia Campus, Virginia Commonwealth University, Richmond, VA, USA.
Virginia Commonwealth University Medical Center · USUniversity of Florida · US

Funding

TRAINING IN THE PHARMACOLOGY OF ABUSED DRUGST32DA007027 · NIDA · VIRGINIA COMMONWEALTH UNIVERSITY · PI William L. Dewey · 1985 to 2026
$14.7M
Targeting of Alpha7 nAChR for therapeutic effectsR01GM057481 · NIGMS · UNIVERSITY OF FLORIDA · PI PAPKE, ROGER L · 2000 to 2023
$7.6M
Genes and molecular pathways in nicotine dependence and withdrawalR01DA032246 · NIDA · VIRGINIA COMMONWEALTH UNIVERSITY · PI DAMAJ, M. IMAD, MILES, MICHAEL F · 2013 to 2017
$1.7M
Role of calcium-dependent mechanisms in nicotine's tolerance and effectsR01DA012610 · NIDA · VIRGINIA COMMONWEALTH UNIVERSITY · PI DAMAJ, M. IMAD · 2001 to 2010
$1.6M
NIDA NIH HHS R01 DA012610NIDA NIH HHS R01 DA032246NIDA NIH HHS R01 DA12610NIDA NIH HHS T32 DA007027NIDA NIH HHS T32 DA007027-41NIGMS NIH HHS R01 GM057481
6 · The paper itself

Abstract

rationaleRecent preclinical data has implicated the α7 nicotinic acetylcholine receptor (nAChR) as a target in modulating nicotine reward. However, the role of the channel properties of the α7 nAChR in nicotine withdrawal is unknown.

objectivesThis study aimed to investigate the impact of α7 nAChR pharmacological modulation on mecamylamine-precipitated nicotine withdrawal behaviors in mice by using positive allosteric modulators (PAMs).

methodsThe effect of the orthosteric α7 nAChR full agonist PNU282987 (1, 3, 9 mg/kg, s.c.), type I α7 PAM NS1738 (1 and 10 mg/kg; i.p.) and the type II α7 PAM PNU120596 (3 and 9 mg/kg, i.p.) on anxiety-like behavior, somatic signs, and hyperalgesia was measured in mice undergoing mecamylamine-precipitated nicotine withdrawal. Mice were infused with 24 mg/kg/day nicotine or saline for 14 days using s.c. osmotic minipumps. Nicotine withdrawal signs were precipitated upon administration of the non-selective nAChR antagonist mecamylamine (3.5 mg/kg, i.p.).

resultsAnxiety-like behavior in nicotine withdrawn mice was only attenuated by PNU282987 in a dose-related fashion. Somatic signs were reduced by PNU282987 and NS1738. PNU120596 was the only compound that reversed precipitated nicotine withdrawal-induced hyperalgesia.

conclusionsTaken together, our results suggest that modulation of the α7 nAChR can play important roles in mecamylamine-precipitated nicotine withdrawal behaviors in mice. In addition, the effects of PAMs in this study suggest that endogenous acetylcholine/choline tone is sufficient to attenuate some aspects of precipitated nicotine withdrawal. These findings highlight a beneficial effect of using α7 nAChR PAMs in some aspects of precipitated nicotine withdrawal.

Indexed as

Disease Models, Animalalpha7 Nicotinic Acetylcholine ReceptorAnimalsBenzamidesBridged Bicyclo CompoundsDose-Response Relationship, DrugInfusion PumpsMaleMecamylamineMiceMice, Inbred ICRNicotineNicotinic AgonistsNicotinic AntagonistsSubstance Withdrawal Syndromealpha7 Nicotinic Acetylcholine ReceptorBenzamidesBridged Bicyclo CompoundsMecamylamineNicotineNicotinic AgonistsNicotinic AntagonistsPNU-282987Mecamylamine-precipitated nicotine withdrawalMouse modelNicotinic acetylcholine receptorPAMs

Identifiers

PMID29549391
PMCPMC6015775
OpenAlexW2790695138

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.