Evidence map›Paper›PMID 19201164›Full record

ArticleEpilepsy research2009

Alpha-1A adrenergic receptor activation increases inhibitory tone in CA1 hippocampus.

Kristin L Hillman, Saobo Lei, Van A Doze, James E Porter

Open access · greenAbstract read
In one paragraph

Article in Epilepsy research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.6field-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

23 citing papers in PubMed, 46 citations in OpenAlex.

  1. Review
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  5. Noradrenergic stimulation of αScientific reports · 2023
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  9. αFrontiers in pharmacology · 2020
    Review
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  12. Review
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
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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

4 authors at 1 institution in 1 country.

Kristin L HillmanDepartment of Pharmacology, Physiology and Therapeutics, University of North Dakota School of Medicine and Health Sciences, 501 North Columbia Road, Grand Forks, ND 58203, United States.
Saobo Lei
Van A Doze
James E Porter
University of North Dakota · US

Funding

TRPC1, CALCIUM AND PARKINSON'S DISEASEP20RR017699 · NCRR · UNIVERSITY OF NORTH DAKOTA · PI GROVE, BRYON D · 2002 to 2011
$19.7M
Inflammatory Signaling Mechanisms of the CGRP ReceptorR21DK062865 · NIDDK · UNIVERSITY OF NORTH DAKOTA · PI PORTER, JAMES · 2003 to 2004
$280k
Molecular Mechanisms Critical to CGRP Receptor SignalingR15GM066726 · NIGMS · UNIVERSITY OF NORTH DAKOTA · PI PORTER, JAMES · 2003 to 2003
$140k
NCRR NIH HHS P20 RR017699NCRR NIH HHS P20RR017699NIDDK NIH HHS R21 DK062865NIGMS NIH HHS R15 GM066726
6 · The paper itself

Abstract

The endogenous catecholamine norepinephrine (NE) exhibits anti-epileptic properties, however it is not well understood which adrenergic receptor (AR) mediates this effect. The aim of this study was to investigate alpha(1)-adrenergic receptor activation in region CA1 of the hippocampus, a subcortical structure often implicated in temporal lobe epilepsies. Using cell-attached and whole-cell recordings in rat hippocampal slices, we confirmed that selective alpha(1)-AR activation increases action potential firing in a subpopulation of CA1 interneurons. We found that this response is mediated via the alpha(1A)-AR subtype, initiated by sodium influx, and appears independent of second messenger signaling. In CA1 pyramidal cells, alpha(1A)-AR activation decreases activity due to increased pre-synaptic GABA and somatostatin release. Examination of post-synaptic receptor involvement revealed that while GABA(A) receptors mediate the majority of alpha(1A)-adrenergic effects on CA1 pyramidal cells, significant contributions are also made by GABA(B) and somatostatin receptors. Finally, to test whether alpha(1A)-AR activation could have potential therapeutic implications, we performed AR agonist challenges using two in vitro epileptiform models. When GABA(A) receptors were available, alpha(1A)-AR activation significantly decreased epileptiform bursting in CA1. Together, our findings directly link stimulation of the alpha(1A)-AR subtype to release of GABA and somatostatin at the single cell level and suggest that alpha(1A)-AR activation may represent one mechanism by which NE exerts anti-epileptic effects within the hippocampus.

Indexed as

Action PotentialsAdrenergic alpha-AgonistsAdrenergic alpha-AntagonistsAnimalsAnimals, NewbornDose-Response Relationship, DrugEvoked PotentialsGABA AntagonistsHippocampusInhibitory Postsynaptic PotentialsIn Vitro TechniquesMaleNeural InhibitionNeuronsOrganophosphorus CompoundsPatch-Clamp Techniques5-methylurapidilAdra1a protein, ratAdrenergic alpha-AgonistsAdrenergic alpha-AntagonistsCGP 35348GABA AntagonistsOrganophosphorus CompoundsPhenylephrinePicrotoxinPiperazinesReceptors, Adrenergic, alpha-1Sodium Channel BlockersSomatostatinTetrodotoxin

Identifiers

PMID19201164
PMCPMC2699218
OpenAlexW2147388330

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.