Evidence map›Paper›PMID 24582613›Full record

ArticleNeuropharmacology2014

Modulation of HCN channels in lateral septum by nicotine.

Sodikdjon A Kodirov, Michael Wehrmeister, Luis V Colom

Open access · greenAbstract read
In one paragraph

Article in Neuropharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

14 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Roles of funny HCN.Comparative biochemistry and physiology. Toxicology & pharmacology : CBP · 2025
    Review
  3. Article
  4. Article
  5. Adam, amigo, brain, and K channel.Biophysical reviews · 2023
    Review
  6. Article
  7. Article
  8. Article
  9. TMEM16B Calcium-Activated Chloride Channels Regulate Action Potential Firing in Lateral Septum and Aggression in Male Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Article
  10. Article
  11. Addictive neurons.Therapeutic targets for neurological diseases · 2017
    Article
  12. Article
  13. Article
  14. HCN Channels Modulators: The Need for Selectivity.Current topics in medicinal chemistry · 2016
    Review
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 2 countries.

Sodikdjon A KodirovCenter for Biomedical Studies, Department of Biological Sciences, University of Texas at Brownsville, TX 78520, USA; Department of Molecular Physiology & Biophysics, University of Iowa, Iowa City, IA 52252, USA. Electronic address: Sodikdjon-Kodirov@uiowa.edu.
Michael WehrmeisterCenter for Biomedical Studies, Department of Biological Sciences, University of Texas at Brownsville, TX 78520, USA; Johannes Gutenberg University, 55099 Mainz, Germany.
Luis V ColomCenter for Biomedical Studies, Department of Biological Sciences, University of Texas at Brownsville, TX 78520, USA.
Johannes Gutenberg University Mainz · DEUniversity of Iowa · US

Funding

Pathophysiology of the septo-hippocampal glutamatergic systemSC1NS065386 · NINDS · UNIV/TEXAS BROWNSVILLE & SOUTHMOST COLL · PI COLOM, LUIS V. · 2008 to 2011
$1.5M
NINDS NIH HHS SC1 NS065386
6 · The paper itself

Abstract

The effects of addictive drugs most commonly occur via interactions with target receptors. The same is true of nicotine and its multiple receptors in a variety of cell types. However, there are also side effects for given substances that can dramatically change cellular, tissue, organ, and organism functions. In this study, we present evidence that nicotine possesses such properties, and modulates neuronal excitability. We recorded whole-cell voltages and currents in neurons situated in the dorsal portion of the lateral septum in acute coronal brain slices of adult rats. Our experiments in the lateral septum revealed that nicotine directly affects HCN - hyperpolarization-activated cyclic nucleotide gated non-selective cation channels. We demonstrate that nicotine effects persist despite the concurrent application of nicotinic acetylcholine receptors' antagonists - mecamylamine, methyllycaconitine, and dihydro-β-erythroidine. These results are novel in regard to HCN channels in the septum, in general, and in their sensitivity to nicotine, in particular.

Indexed as

Action PotentialsAnimalsBiophysical PhenomenaBiophysicsCyclic Nucleotide-Gated Cation ChannelsDihydro-beta-ErythroidineElectric StimulationIn Vitro TechniquesMecamylamineNeuronsNicotineNicotinic AgonistsNicotinic AntagonistsPatch-Clamp TechniquesRatsRats, Sprague-DawleyCyclic Nucleotide-Gated Cation ChannelsDihydro-beta-ErythroidineMecamylamineNicotineNicotinic AgonistsNicotinic AntagonistsAction potentialsHCN channelsh-CurrentSag potentialSeptal neurons

Identifiers

PMID24582613
PMCPMC5384640
OpenAlexW2123603025

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.