Evidence map›Paper›PMID 18971298›Full record

ArticleJournal of neurophysiology2009

Developmental sensitivity of hippocampal interneurons to ethanol: involvement of the hyperpolarization-activated current, Ih.

Haidun Yan, Qiang Li, Rebekah Fleming, Roger D Madison, Wilkie A Wilson, H Scott Swartzwelder

Abstract read
In one paragraph

Article in Journal of neurophysiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
1.7field-weighted citation impact, top 19% 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

31 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. HCN Channel Targets for Novel Antidepressant Treatment.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2017
    Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Neuroimmune Function and the Consequences of Alcohol Exposure.Alcohol research : current reviews · 2015
    Review
  15. Review
  16. Review
  17. Neuroimmune basis of alcoholic brain damage.International review of neurobiology · 2014
    Review
  18. Article
  19. Article
  20. 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

6 authors at 1 institution in 1 country.

Haidun YanDepartment of Psychiatry, Duke University Medical Center, Durham, NC, USA.
Qiang Li
Rebekah Fleming
Roger D Madison
Wilkie A Wilson
H Scott Swartzwelder
Duke Medical Center · US

Funding

Ethanol and GABA Function: Developmental SensitivityR01AA014894 · NIAAA · DUKE UNIVERSITY · PI SWARTZWELDER, H SCOTT · 2005 to 2008
$1.1M
NIAAA NIH HHS AA-014894
6 · The paper itself

Abstract

Ethanol (EtOH) has powerful effects on GABA(A) receptor-mediated neurotransmission, and we have previously shown that EtOH-induced enhancement of GABA(A) receptor-mediated synaptic transmission in the hippocampus is developmentally regulated. Because synaptic inhibition is determined in part by the firing properties of interneurons, we have investigated the mechanisms whereby EtOH influences the spontaneous firing characteristics and hyperpolarization-activated cation current (Ih) of hippocampal interneurons located in the near to the border of stratum lacunosum moleculare and s. radiatum of adolescent and adult rats. EtOH did not affect current injection-induced action potentials of interneurons that do not exhibit spontaneous firing. However, in neurons that fire spontaneously, EtOH enhanced the frequency of spontaneous action potentials (sAPs) in a concentration-dependent manner, an effect that was more pronounced in interneurons from adolescent rats, compared with adult rats. EtOH also modulated the afterhyperpolarization (AHP) that follows sAPs by shortening the tau(slow) decay time constant, and this effect was more pronounced in slices from adolescent rats. EtOH increased Ih amplitudes, accelerated Ih activation kinetics, and increased the maximal Ih conductance in interneurons from animals in both age groups. These effects were also more pronounced in interneurons from adolescents and persisted in the presence of glutamatergic and GABAergic blockers. However, EtOH failed to affect sAP firing in the presence of ZD7288 or cesium chloride. These results suggest that Ih may be of mechanistic significance in the effect of EtOH on interneuron spontaneous firing.

Indexed as

Action PotentialsAgingAnimalsCentral Nervous System DepressantsCesiumChloridesCyclic Nucleotide-Gated Cation ChannelsData Interpretation, StatisticalElectrophysiologyEthanolGABA AntagonistsGlutamic AcidHippocampusHyperpolarization-Activated Cyclic Nucleotide-Gated ChannelsInterneuronsMaleCentral Nervous System DepressantsCesiumcesium chlorideChloridesCyclic Nucleotide-Gated Cation ChannelsEthanolGABA AntagonistsGlutamic AcidHyperpolarization-Activated Cyclic Nucleotide-Gated ChannelsICI D2788Potassium ChannelsPyrimidines

Identifiers

PMID18971298
PMCPMC2637011
OpenAlexW2007324843

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.