Evidence map›Paper›PMID 38902419›Full record

ArticleScientific reports2024

Abundant extrasynaptic expression of α3β4-containing nicotinic acetylcholine receptors in the medial habenula-interpeduncular nucleus pathway in mice.

Asuka Tsuzuki, Miwako Yamasaki, Kohtarou Konno, Taisuke Miyazaki, Norio Takei, Susumu Tomita, Michisuke Yuzaki, Masahiko Watanabe

Abstract read
In one paragraph

Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Article
  2. Review
  3. 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

8 authors.

Asuka Tsuzuki *Department of Anatomy, Graduate School of Medicine, Hokkaido University, Sapporo, 060-8638, Japan.
Miwako Yamasaki *Department of Anatomy, Faculty of Medicine, Hokkaido University, Sapporo, 060-8638, Japan. k-minobe@med.hokudai.ac.jp.
Kohtarou KonnoDepartment of Anatomy, Faculty of Medicine, Hokkaido University, Sapporo, 060-8638, Japan.
Taisuke MiyazakiDepartment of Functioning and Disability, Faculty of Health Sciences, Hokkaido University, Sapporo, 060-8638, Japan.
Norio TakeiInstitute for Animal Experimentation, Faculty of Medicine, Hokkaido University, Sapporo, 060-8638, Japan.
Susumu TomitaDepartment of Cellular and Molecular Physiology, Department of Neuroscience, and Kavli Institute for Neuroscience, Yale University School of Medicine, New Haven, CT, 06520, USA.
Michisuke YuzakiDepartment of Physiology, School of Medicine, Keio University, Tokyo, 160-8582, Japan.
Masahiko WatanabeDepartment of Anatomy, Faculty of Medicine, Hokkaido University, Sapporo, 060-8638, Japan.

Funding

Ministry of Education, Culture, Sports, Science and Technology 17KK0160Ministry of Education, Culture, Sports, Science and Technology 20H05628Ministry of Education, Culture, Sports, Science and Technology 21K06746Ministry of Education, Culture, Sports, Science and Technology 22K06784
6 · The paper itself

Abstract

Nicotinic acetylcholine receptors (nAChRs) in the medial habenula (MHb)-interpeduncular nucleus (IPN) pathway play critical roles in nicotine-related behaviors. This pathway is particularly enriched in nAChR α3 and β4 subunits, both of which are genetically linked to nicotine dependence. However, the cellular and subcellular expression of endogenous α3β4-containing nAChRs remains largely unknown because specific antibodies and appropriate detection methods were unavailable. Here, we successfully uncovered the expression of endogenous nAChRs containing α3 and β4 subunits in the MHb-IPN pathway using novel specific antibodies and a fixative glyoxal that enables simultaneous detection of synaptic and extrasynaptic molecules. Immunofluorescence and immunoelectron microscopy revealed that both subunits were predominantly localized to the extrasynaptic cell surface of somatodendritic and axonal compartments of MHb neurons but not at their synaptic junctions. Immunolabeling for α3 and β4 subunits disappeared in α5β4-knockout brains, which we used as negative controls. The enriched and diffuse extrasynaptic expression along the MHb-IPN pathway suggests that α3β4-containing nAChRs may enhance the excitability of MHb neurons and neurotransmitter release from their presynaptic terminals in the IPN. The revealed distribution pattern provides a molecular and anatomical basis for understanding the functional role of α3β4-containing nAChRs in the crucial pathway of nicotine dependence.

Indexed as

HabenulaInterpeduncular NucleusReceptors, NicotinicAnimalsMaleMiceMice, Inbred C57BLMice, KnockoutNerve Tissue ProteinsNeuronsSynapsesChrnb4 protein, mouseNerve Tissue Proteinsnicotinic receptor alpha3beta4Receptors, Nicotinic

Identifiers

PMID38902419
PMCPMC11189931

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Registered trials

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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.