Evidence map›Paper›PMID 20236223›Full record

ArticleJournal of neurochemistry2010

Stimulation of lateral hypothalamic glutamate and acetylcholine efflux by nicotine: implications for mechanisms of nicotine-induced activation of orexin neurons.

Ravi K Pasumarthi, Jim Fadel

Open access · bronzeAbstract read
In one paragraph

Article in Journal of neurochemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

15 citing papers in PubMed, 29 citations in OpenAlex.

  1. 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
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  13. Nicotinic regulation of energy homeostasis.Nicotine & tobacco research : official journal of the Society for Research on Nicotine and Tobacco · 2012
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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

2 authors at 1 institution in 1 country.

Ravi K PasumarthiDepartment of Pharmacology, Physiology and Neuroscience, University of South Carolina School of Medicine, Columbia, South Carolina 29208, USA.
Jim Fadel
University of South Carolina · US

Funding

Aging, acetylcholine and the hypothalamusR01AG030646 · NIA · UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA · PI FADEL, JIM R · 2008 to 2011
$1.2M
NIA NIH HHS R01 AG030646NIA NIH HHS R01AG030646
6 · The paper itself

Abstract

The hypothalamus is a prominent target of nicotine action. We have previously shown that acute systemic nicotine treatment induces Fos expression in the lateral hypothalamus and perifornical area (LH/PFA), with orexin/hypocretin neurons being particularly responsive. However, the neurochemical correlates of acute nicotine treatment in the LH/PFA have not been described. Anatomical studies have revealed that this area receives afferents from cholinergic, glutamatergic, and GABAergic telencephalic brain regions, suggesting a potential role for these neurotransmitters in mediating the hypothalamic component of nicotine effects on homeostatic phenomena, such as arousal and appetite. Here, we used in vivo microdialysis to determine the effect of acute systemic or local nicotine on glutamate, acetylcholine, and GABA efflux in the LH/PFA of rats. Local administration of nicotine significantly increased acetylcholine and glutamate, but not GABA, in the LH/PFA. Thus, we further tested the role of afferent sources of glutamate and acetylcholine in mediating acute nicotine-induced activation of orexin neurons by unilaterally lesioning the prefrontal cortex or basal forebrain cholinergic regions. Lesioned animals showed reduced Fos-positive orexin neurons following nicotine treatment. These data suggest that both acetylcholine and glutamate may mediate the effects of acute nicotine on the activity of hypothalamic neurons, including orexin/hypocretin cells. Changes in cholinergic or glutamatergic transmission in this region with chronic nicotine may contribute to long-term alterations in functions mediated by LH/PFA neurons, including feeding and arousal.

Indexed as

AcetylcholineAnimalsAppetiteArousalDrug Administration ScheduleExtracellular Fluidgamma-Aminobutyric AcidGlutamic AcidHypothalamic Area, LateralIntracellular Signaling Peptides and ProteinsMaleMicrodialysisNeural PathwaysNeuronsNeuropeptidesNicotineAcetylcholinegamma-Aminobutyric AcidGlutamic AcidIntracellular Signaling Peptides and ProteinsNeuropeptidesNicotineNicotinic AgonistsOrexins

Identifiers

PMID20236223
PMCPMC2860645
OpenAlexW2067885578

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.