Evidence map›Paper›PMID 29908238›Full record

ArticleNeuropharmacology2018

Small conductance calcium activated potassium (SK) channel dependent and independent effects of riluzole on neuropathic pain-related amygdala activity and behaviors in rats.

Jeremy M Thompson, Vadim Yakhnitsa, Guangchen Ji, Volker Neugebauer

Open access · greenAbstract read
In one paragraph

Article in Neuropharmacology, 2018. 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
1.2field-weighted citation impact, top 21% 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, 25 citations in OpenAlex.

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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.

Jeremy M ThompsonDepartment of Pharmacology and Neuroscience, Texas Tech University Health Sciences Center, School of Medicine, Lubbock, TX, USA.
Vadim YakhnitsaDepartment of Pharmacology and Neuroscience, Texas Tech University Health Sciences Center, School of Medicine, Lubbock, TX, USA.
Guangchen JiDepartment of Pharmacology and Neuroscience, Texas Tech University Health Sciences Center, School of Medicine, Lubbock, TX, USA.
Volker NeugebauerDepartment of Pharmacology and Neuroscience, Texas Tech University Health Sciences Center, School of Medicine, Lubbock, TX, USA; Center of Excellence for Translational Neuroscience and Therapeutics, Texas Tech University Health Sciences Center, Lubbock, TX, USA. Electronic address: volker.neugebauer@ttuhsc.edu.
Texas Tech University · US

Funding

PAIN, NOCICEPTION, AND THE AMYGDALAR01NS038261 · NINDS · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI Volker Neugebauer, Igor Ponomarev · 1999 to 2026
$8.7M
Stress-induced descending facilitation from amygdala kappa opioid receptors in functional painR01NS106902 · NINDS · UNIVERSITY OF ARIZONA · PI NEUGEBAUER, VOLKER, PORRECA, FRANK · 2018 to 2022
$2.7M
Amygdala Serotonin Neurotransmission and Neuropathic PainR01NS081121 · NINDS · UNIVERSITY OF TEXAS MED BR GALVESTON · PI GREEN, THOMAS ARTHUR, NEUGEBAUER, VOLKER · 2013 to 2017
$2.3M
NINDS NIH HHS R01 NS038261NINDS NIH HHS R01 NS081121NINDS NIH HHS R01 NS106902
6 · The paper itself

Abstract

background and purposeChronic neuropathic pain is an important healthcare issue with significant emotional components. The amygdala is a brain region involved in pain and emotional-affective states and disorders. The central amygdala output nucleus (CeA) contains small-conductance calcium-activated potassium (SK) channels that can control neuronal activity. A clinically available therapeutic, riluzole can activate SK channels and may have antinociceptive effects through a supraspinal action. We tested the hypothesis that riluzole inhibits neuropathic pain behaviors by inhibiting pain-related changes in CeA neurons, in part at least through SK channel activation. EXPERIMENTAL APPROACH: Brain slice physiology and behavioral assays were done in adult Sprague Dawley rats. Audible and ultrasonic vocalizations and von Frey thresholds were measured in sham and neuropathic rats 4 weeks after left L5 spinal nerve ligation (SNL model). Whole cell patch-clamp recordings of regular firing CeA neurons in brain slices were used to measure synaptic transmission and neuronal excitability. KEY

resultsIn brain slices, riluzole increased the SK channel-mediated afterhyperpolarization and synaptic inhibition, but inhibited neuronal excitability through an SK channel independent action. SNL rats had increased vocalizations and decreased withdrawal thresholds compared to sham rats, and intra-CeA administration of riluzole inhibited vocalizations and depression-like behaviors but did not affect withdrawal thresholds. Systemic riluzole administration also inhibited these changes, demonstrating the clinical utility of this strategy. SK channel blockade in the CeA attenuated the inhibitory effects of systemic riluzole on vocalizations, confirming SK channel involvement in these effects. CONCLUSIONS AND IMPLICATIONS: The results suggest that riluzole has beneficial effects on neuropathic pain behaviors through SK channel dependent and independent mechanisms in the amygdala.

Indexed as

Analgesics, Non-NarcoticAnimalsCentral Amygdaloid NucleusDisease Models, AnimalMaleMembrane PotentialsNeuralgiaNeural InhibitionNeurotransmitter AgentsPain ThresholdRandom AllocationRats, Sprague-DawleyRiluzoleSmall-Conductance Calcium-Activated Potassium ChannelsSpinal NervesSynaptic TransmissionAnalgesics, Non-NarcoticNeurotransmitter AgentsRiluzoleSmall-Conductance Calcium-Activated Potassium ChannelsAmygdalaBehaviorElectrophysiologyNeuropathic painRiluzoleSK channels

Identifiers

PMID29908238
PMCPMC6070350
OpenAlexW2808113489

What OpenQuestion holds

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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.