Evidence map›Paper›PMID 16319313›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2005

Cholinergic modulation of appetite-related synapses in mouse lateral hypothalamic slice.

Young-Hwan Jo, Denise Wiedl, Lorna W Role

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.1field-weighted citation impact, top 28% 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

25 citing papers in PubMed, 51 citations in OpenAlex.

  1. Article
  2. Article
  3. Mechanisms of Nicotine Addiction.Cold Spring Harbor perspectives in medicine · 2021
    Review
  4. Article
  5. Nicotinic Acetylcholine Receptor Signaling in the Hypothalamus: Mechanisms Related to Nicotine's Effects on Food Intake.Nicotine & tobacco research : official journal of the Society for Research on Nicotine and Tobacco · 2020
    Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. Molecular mechanisms underlying behaviors related to nicotine addiction.Cold Spring Harbor perspectives in medicine · 2013
    Review
  14. Review
  15. Nicotinic regulation of energy homeostasis.Nicotine & tobacco research : official journal of the Society for Research on Nicotine and Tobacco · 2012
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

3 authors at 1 institution in 1 country.

Young-Hwan JoDepartment of Anatomy and Cell Biology, Center for Neurobiology and Behavior, Columbia University, College of Physicians and Surgeons, New York, New York 10032, USA.
Denise Wiedl
Lorna W Role
Columbia University · US

Funding

MODULATORY EFFECTS OF SUBSTANCE P ON AUTONOMIC NEURONSR01NS022061 · NINDS · STATE UNIVERSITY NEW YORK STONY BROOK · PI PLOTKIN, JOSHUA L · 1985 to 2019
$9.6M
NINDS NIH HHS NS22061NINDS NIH HHS R01 NS022061
6 · The paper itself

Abstract

Nicotine administration reduces appetite and alters feeding patterns; a major deterrent to smoking cessation is hyperphagia and resultant weight gain. We demonstrate here that lateral hypothalamic (LH) circuits involving melanin-concentrating hormone (MCH) neurons are subject to cholinergic modulation that may be related to the effects of nicotine on appetite control. Cholinergic input to the perifornical LH area of the mouse is confirmed by examination of immunostaining for vesicular acetylcholine (ACh) transporter (VAT) in conjunction with antibodies to MCH and the vesicular GABA transporter (vGABAT). vAChT-positive neurons border the LH, and VAT-positive projections are detected throughout the perifornical area. MCH-positive dendrites appear studded with vGABAT-positive contacts, consistent with recordings of GABAergic inputs to LH/MCH neurons identified by their location, morphology, electrophysiological profile, and MCH expression. Activation of presynaptic nicotinic ACh receptors (nAChRs) enhances GABAergic transmission. GABAergic transmission is potentiated by (1) direct nicotine application, (2) increasing local ACh concentration, and (3) stimulation of cholinergic projections. Based on pharmacological studies and comparisons of wild-type versus alpha7 nAChR subunit mutant mice, we propose that alpha7*-nAChRs are required for the modulation of GABAergic inputs in LH. Prenatal exposure to nicotine elicits a persistent elevation of GABAergic transmission in the LH of postnatal pups. Furthermore, GABAergic inputs to LH of prenatal nicotine-exposed pups are insensitive to subsequent nicotine challenge. Our studies support the hypothesis that nicotine administration or elevated cholinergic tone enhance inhibition of perifonical LH/MCH neurons via activation of presynaptic alpha7*-nAChRs.

Indexed as

Acetylcholinealpha7 Nicotinic Acetylcholine ReceptorAnimalsAnimals, NewbornAppetiteCholinergic FibersFemalegamma-Aminobutyric AcidHypothalamic Area, LateralHypothalamic HormonesIn Vitro TechniquesMelaninsMiceMice, Inbred C57BLMice, KnockoutNeural InhibitionAcetylcholinealpha7 Nicotinic Acetylcholine ReceptorChrna7 protein, mousegamma-Aminobutyric AcidHypothalamic Hormonesmelanin-concentrating hormoneMelaninsNicotinePituitary HormonesReceptors, CholinergicReceptors, Nicotinic

Identifiers

PMID16319313
PMCPMC2280035
OpenAlexW1967554536

What OpenQuestion holds

Textmetadata
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.