Evidence map›Paper›PMID 24653701›Full record

ArticleFrontiers in pharmacology2014

Identification of both GABAA receptors and voltage-activated Na(+) channels as molecular targets of anticonvulsant α-asarone.

Ze-Jun Wang, Simon R Levinson, Liqin Sun, Thomas Heinbockel

Open access · goldAbstract read
In one paragraph

Article in Frontiers in pharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
6.1field-weighted citation impact, top 5% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.

  1. Pooled it
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  7. Article
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  11. Therapeutic Potential of Active Components fromJournal of pharmacopuncture · 2022
    Review
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  16. Role of Vacha (Journal of clinical medicine · 2020
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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 2 institutions in 1 country.

Ze-Jun WangDepartment of Anatomy, College of Medicine, Howard University Washington, DC, USA.
Simon R LevinsonDepartment of Physiology and Biophysics, University of Colorado Denver School of Medicine Aurora, CO, USA.
Liqin SunDepartment of Anatomy, College of Medicine, Howard University Washington, DC, USA.
Thomas HeinbockelDepartment of Anatomy, College of Medicine, Howard University Washington, DC, USA.
Howard University · USUniversity of Colorado Denver · US

Funding

Sleep Disorders in Adults with Sickle Cell Disease: Frequency, Associations with Cardiovascular and Pain Indicators, and Responses to TreatmentU54MD007597 · NIMHD · HOWARD UNIVERSITY · PI BYRON D. FORD · 2019 to 2026
$37.7M
The Howard University SCORE Program Supplemental GrantS06GM008016 · NIGMS · HOWARD UNIVERSITY · PI WALCOURT, ASIKIYA · 1989 to 2009
$16.1M
PROTEOMICS CORE FACILITYG12MD007597 · NIMHD · HOWARD UNIVERSITY · PI SOUTHERLAND, WILLIAM M. · 2012 to 2018
$14.8M
NIGMS NIH HHS S06 GM008016NIMHD NIH HHS G12 MD007597NIMHD NIH HHS U54 MD007597
6 · The paper itself

Abstract

Alpha (α)-asarone, a major effective component isolated from the Chinese medicinal herb Acorus tatarinowii, is clinically used as medication for treating epilepsy, cough, bronchitis, and asthma. In the present study, we demonstrated that α-asarone targets central nervous system GABAA receptor as well as voltage-gated Na(+) channels. Using whole-cell patch-clamp recording, α-asarone inhibited spontaneous firing of output neurons, mitral cells (MCs), in mouse olfactory bulb brain slice preparation and hyperpolarized the membrane potential of MCs. The inhibitory effect of α-asarone persisted in the presence of ionotropic glutamate receptor blockers but was eliminated after adding a GABAA receptor blocker, suggesting that GABAA receptors mediated the inhibition of MCs by α-asarone. This hypothesis was supported by the finding that α-asarone evoked an outward current, but did not influence inhibitory postsynaptic currents (IPSCs). In addition to inhibiting spontaneous firing, α-asarone also inhibited the Nav1.2 channel, a dominant rat brain Na(+) channel subtype. The effects of α-asarone on a defined Nav1.2 were characterized using transfected cells that stably expressed the Nav1.2 channel isoform. α-Asarone displayed strong tonic inhibition of Nav1.2 currents in a concentration- and membrane potential-dependent fashion. α-Asarone reduced channel availability in steady-state inactivation protocols by enhancing or stabilizing Na(+) channel inactivation. Both Na(+) channel blockade and activation of GABAA receptors provide a possible mechanism for the known anti-epileptic effects of α-asarone. It also suggests that α-asarone could benefit patients with cough possibly through inhibiting a Na(+) channel subtype to inhibit peripheral and/or central sensitization of cough reflexes.

Indexed as

anticonvulsantcentral nerve Nav1.2 channelGABAA receptorsolfactory bulbsensitization of cough reflexessodium channel blockerα-asarone

Identifiers

PMID24653701
PMCPMC3949418
OpenAlexW2123050819

What OpenQuestion holds

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Registered trials

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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.