Evidence map›Paper›PMID 33216167›Full record

ArticlePsychopharmacology2021

Nicotinic receptor modulation of the default mode network.

Britta Hahn, Alexander N Harvey, Marta Concheiro-Guisan, Marilyn A Huestis, Thomas J Ross, Elliot A Stein

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

Article in Psychopharmacology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.2field-weighted citation impact, top 49% 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

8 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. Role of Cholinergic Signaling in Alzheimer's Disease.Molecules (Basel, Switzerland) · 2022
    Review
  7. Review
  8. Article
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

6 authors at 2 institutions in 1 country.

Britta HahnUniversity of Maryland School of Medicine, Maryland Psychiatric Research Center, P.O. Box 21247, Baltimore, MD, 21228, USA. bhahn@som.umaryland.edu.ORCID http://orcid.org/0000-0002-0709-4543
Alexander N HarveyUniversity of Maryland School of Medicine, Maryland Psychiatric Research Center, P.O. Box 21247, Baltimore, MD, 21228, USA.
Marta Concheiro-GuisanNeuroimaging Research Branch, National Institute on Drug Abuse Intramural Research Program, 251 Bayview Blvd, Suite 200, Baltimore, MD, 21224, USA.
Marilyn A HuestisNeuroimaging Research Branch, National Institute on Drug Abuse Intramural Research Program, 251 Bayview Blvd, Suite 200, Baltimore, MD, 21224, USA.
Thomas J RossNeuroimaging Research Branch, National Institute on Drug Abuse Intramural Research Program, 251 Bayview Blvd, Suite 200, Baltimore, MD, 21224, USA.
Elliot A SteinNeuroimaging Research Branch, National Institute on Drug Abuse Intramural Research Program, 251 Bayview Blvd, Suite 200, Baltimore, MD, 21224, USA.
National Institute on Drug Abuse · USUniversity of Maryland, Baltimore · US

Funding

Functional and Structural Brain Circuits Underlying SmokingZIADA000573 · NIDA · NATIONAL INSTITUTE ON DRUG ABUSE · PI STEIN, ELLIOT A · 2010 to 2021
$19.4M
Nicotinic modulation of the default network of resting brain functionR21DA027894 · NIDA · UNIVERSITY OF MARYLAND BALTIMORE · PI HAHN, BRITTA · 2010 to 2011
$407k
NIDA NIH HHS R21 DA027894
6 · The paper itself

Abstract

rationalePrevious neuroimaging studies of cognition involving nicotinic acetylcholine receptor (nAChR) agonist administration have repeatedly found enhanced task-induced deactivation of regions of the default mode network (DMN), a group of brain systems that is more active at rest and mediates task-independent thought processes. This effect may be related to pro-cognitive nAChR agonist effects

objectivesThe present study sought to test whether nAChR modulation of the DMN is bi-directional, i.e., whether a nAChR antagonist would reduce task-induced deactivation.

methodsEighteen healthy non-smokers underwent functional magnetic resonance imaging while performing a letter N-back task. Scans were performed after nicotine administration (7 mg/24 h, transdermally), after administration of the nAChR antagonist mecamylamine (7.5 mg, p.o.), and after double placebo, in counterbalanced sequence. Blood-oxygen-level-dependent (BOLD) signal was analyzed within ventromedial prefrontal cortex (vmPFC) and posterior cingulate cortex (PCC) regions of interest-central hubs of the DMN in which consistent nAChR agonist-induced changes had previously been identified.

resultsNicotine enhanced hit rate in both the 0-back and 2-back condition, while mecamylamine slowed reaction time in the 2-back condition. Mecamylamine reduced task-induced deactivation of vmPFC and PCC. Nicotine had no significant effects on the BOLD signal.

conclusionsThe finding that nAChR tone reduction by mecamylamine weakened task-induced DMN deactivation indicates that a constant tone of nAChR activation helps regulate DMN activity in healthy individuals. This suggests that low nAChR tone may play a causal role in DMN dysregulation seen in conditions such as mild cognitive impairment or Alzheimer's disease.

Indexed as

Magnetic Resonance ImagingAdultBrainCognitionCognitive DysfunctionDefault Mode NetworkFemaleGyrus CinguliHumansMaleMecamylamineMiddle AgedNicotineNicotinic AgonistsNicotinic AntagonistsPrefrontal CortexMecamylamineNicotineNicotinic AgonistsNicotinic AntagonistsReceptors, NicotinicCognitionDeactivationDefault mode networkfMRIMecamylamineN-backNicotineNicotinic acetylcholine receptor

Identifiers

PMID33216167
PMCPMC11683817
OpenAlexW3098535416

What Socratic 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 Socratic graph.