Evidence map›Paper›PMID 25691360›Full record

ArticleEuropean journal of pain (London, England)2015

Nerve injury-induced calcium channel alpha-2-delta-1 protein dysregulation leads to increased pre-synaptic excitatory input into deep dorsal horn neurons and neuropathic allodynia.

C Zhou, Z D Luo

Abstract read
In one paragraph

Article in European journal of pain (London, England), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 10% 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

34 citing papers in PubMed, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.

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  11. Insula→Amygdala and Insula→Thalamus Pathways Are Involved in Comorbid Chronic Pain and Depression-Like Behavior in Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
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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

2 authors at 1 institution in 1 country.

C ZhouDepartment of Pharmacology, School of Medicine, University of California Irvine, USA.
Z D LuoDepartment of Pharmacology, School of Medicine, University of California Irvine, USA.
University of California, Irvine · US

Funding

A novel pathway mediating the development of chronic orofacial neuropathic painR01DE021847 · NIDCR · UNIVERSITY OF CALIFORNIA-IRVINE · PI LUO, ZHIGANG DAVID, STEWARD, OSWALD · 2011 to 2015
$3.6M
Mechanism of Calcium Channel Cava2d1 Protein Mediated Neuropathic PainR01NS064341 · NINDS · UNIVERSITY OF CALIFORNIA-IRVINE · PI LUO, ZHIGANG DAVID · 2010 to 2013
$1.2M
CALCIUM CHANNEL SUBUNIT REGULATION AND NEUROPATHIC PAINR01NS040135 · NINDS · UNIVERSITY OF CALIFORNIA SAN DIEGO · PI LUO, ZHIGANG DAVID · 2001 to 2005
$1.1M
NIDCR NIH HHS DE021847NIDCR NIH HHS R01 DE021847NINDS NIH HHS NS064341NINDS NIH HHS NS40135NINDS NIH HHS R01 NS040135NINDS NIH HHS R01 NS064341
6 · The paper itself

Abstract

backgroundUp-regulation of voltage-gated calcium channel α2 δ1 subunit post spinal nerve ligation (SNL) injury or in α2 δ1 -overexpressing transgenic (Tg) mice correlates with tactile allodynia, a pain state mediated mainly by Aβ sensory fibres forming synaptic connections with deep dorsal horn (DDH) neurons. It is not clear, however, whether dysregulated α2 δ1 alters DDH synaptic neurotransmission that underlies tactile allodynia development post nerve injury.

methodsTactile allodynia was tested in the SNL and α2 δ1 Tg models. Miniature excitatory/inhibitory post-synaptic currents were recorded in DDH neurons from these animal models using whole-cell patch clamp slice recording techniques.

resultsThere was a significant increase in the frequency, but not amplitude, of miniature excitatory post-synaptic currents (mEPSC) in DDH neurons that correlated with tactile allodynia in SNL and α2 δ1 Tg mice. Gabapentin, an α2 δ1 ligand that is known to block tactile allodynia in these models, also normalized mEPSC frequency dose-dependently in DDH neurons from SNL and α2 δ1 Tg mice. In contrast, neither frequency nor amplitude of miniature inhibitory post-synaptic currents was altered in DDH neurons from SNL and α2 δ1 Tg mice.

conclusionOur data suggest that α2 δ1 dysregulation is highly likely contributing to tactile allodynia through a pre-synaptic mechanism involving facilitation of excitatory synaptic neurotransmission in DDH of spinal cord.

Indexed as

HyperalgesiaNeuralgiaPeripheral Nerve InjuriesAnimalsCalcium ChannelsDisease Models, AnimalExcitatory Postsynaptic PotentialsMaleMiceMice, TransgenicPosterior Horn CellsSpinal NervesTouch PerceptionUp-RegulationCACNA2D1 protein, mouseCalcium Channels

Identifiers

PMID25691360
PMCPMC4539283
OpenAlexW2018700436

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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.