Evidence map›Paper›PMID 29468190›Full record

ArticleeNeuro

Optogenetic Activation of Non-Nociceptive Aβ Fibers Induces Neuropathic Pain-Like Sensory and Emotional Behaviors after Nerve Injury in Rats.

Ryoichi Tashima, Keisuke Koga, Misuzu Sekine, Kensho Kanehisa, Yuta Kohro, Keiko Tominaga, Katsuyuki Matsushita, Hidetoshi Tozaki-Saitoh, Yugo Fukazawa, Kazuhide Inoue and 3 more

Open access · goldAbstract read
In one paragraph

Article in eNeuro. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
4.1field-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

44 citing papers in PubMed, 79 citations in OpenAlex.

  1. Article
  2. Article
  3. Spinal Processing of Spatiotemporally Diverse Tactile Stimuli: Computational Insights into Allodynia and Spinal Cord Stimulation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026
    Article
  4. Article
  5. Article
  6. Review
  7. BH4 Oxidation-Derived HJournal of neurochemistry · 2025
    Article
  8. Article
  9. Gene therapy for chronic pain management.Cell reports. Medicine · 2024
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Optogenetic and Chemogenic Control of Pain Signaling: Molecular Markers.International journal of molecular sciences · 2023
    Review
  20. Article
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

13 authors at 4 institutions in 1 country.

Ryoichi TashimaDepartment of Life Innovation, Graduate School of Pharmaceutical Sciences, Kyushu University, Fukuoka 812-8582, Japan.
Keisuke KogaDepartment of Life Innovation, Graduate School of Pharmaceutical Sciences, Kyushu University, Fukuoka 812-8582, Japan.ORCID 0000-0003-3729-3030
Misuzu SekineDepartment of Life Innovation, Graduate School of Pharmaceutical Sciences, Kyushu University, Fukuoka 812-8582, Japan.
Kensho KanehisaDepartment of Life Innovation, Graduate School of Pharmaceutical Sciences, Kyushu University, Fukuoka 812-8582, Japan.
Yuta KohroDepartment of Life Innovation, Graduate School of Pharmaceutical Sciences, Kyushu University, Fukuoka 812-8582, Japan.
Keiko TominagaDepartment of Molecular and System Pharmacology, Graduate School of Pharmaceutical Sciences, Kyushu University, Fukuoka 812-8582, Japan.
Katsuyuki MatsushitaDepartment of Molecular and System Pharmacology, Graduate School of Pharmaceutical Sciences, Kyushu University, Fukuoka 812-8582, Japan.
Hidetoshi Tozaki-SaitohDepartment of Life Innovation, Graduate School of Pharmaceutical Sciences, Kyushu University, Fukuoka 812-8582, Japan.
Yugo FukazawaDepartment of Brain Structure and Function, Research Center for Child Mental Development, Faculty of Medical Sciences, University of Fukui, Fukui 910-1193, Japan.ORCID 0000-0001-7436-8797
Kazuhide InoueDepartment of Molecular and System Pharmacology, Graduate School of Pharmaceutical Sciences, Kyushu University, Fukuoka 812-8582, Japan.
Hiromu YawoDepartment of Developmental Biology and Neuroscience, Tohoku University Graduate School of Life Sciences, Sendai, Miyagi 980-8577, Japan.ORCID 0000-0002-4299-3288
Hidemasa FurueDepartment of Neurophysiology, Hyogo College of Medicine, Nishinomiya, Hyogo 663-8501, Japan.
Makoto TsudaDepartment of Life Innovation, Graduate School of Pharmaceutical Sciences, Kyushu University, Fukuoka 812-8582, Japan.ORCID 0000-0003-0585-9570
Kyushu University · JPHyogo Medical University · JPTohoku University · JPUniversity of Fukui · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neuropathic pain is caused by peripheral nerve injury (PNI). One hallmark symptom is allodynia (pain caused by normally innocuous stimuli), but its mechanistic underpinning remains elusive. Notably, whether selective stimulation of non-nociceptive primary afferent Aβ fibers indeed evokes neuropathic pain-like sensory and emotional behaviors after PNI is unknown, because of the lack of tools to manipulate Aβ fiber function in awake, freely moving animals. In this study, we used a transgenic rat line that enables stimulation of non-nociceptive Aβ fibers by a light-activated channel (channelrhodopsin-2; ChR2). We found that illuminating light to the plantar skin of these rats with PNI elicited pain-like withdrawal behaviors that were resistant to morphine. Light illumination to the skin of PNI rats increased the number of spinal dorsal horn (SDH) Lamina I neurons positive to activity markers (c-Fos and phosphorylated extracellular signal-regulated protein kinase; pERK). Whole-cell recording revealed that optogenetic Aβ fiber stimulation after PNI caused excitation of Lamina I neurons, which were normally silent by this stimulation. Moreover, illuminating the hindpaw of PNI rats resulted in activation of central amygdaloid neurons and produced an aversion to illumination. Thus, these findings provide the first evidence that optogenetic activation of primary afferent Aβ fibers in PNI rats produces excitation of Lamina I neurons and neuropathic pain-like behaviors that were resistant to morphine treatment. This approach may provide a new path for investigating circuits and behaviors of Aβ fiber-mediated neuropathic allodynia with sensory and emotional aspects after PNI and for discovering novel drugs to treat neuropathic pain.

Indexed as

AnimalsAvoidance LearningChannelrhodopsinsConditioning, PsychologicalDisease Models, AnimalEmotionsExtracellular Signal-Regulated MAP KinasesGanglia, SpinalLumbar VertebraeMaleNeuralgiaNeurons, AfferentOptogeneticsPatch-Clamp TechniquesProto-Oncogene Proteins c-fosRats, TransgenicChannelrhodopsinsExtracellular Signal-Regulated MAP KinasesProto-Oncogene Proteins c-fosaversionAβ fibersneuropathic painoptogeneticsprimary afferentsspinal cord

Identifiers

PMID29468190
PMCPMC5819669
OpenAlexW2789504405

What OpenQuestion holds

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LicenceCC BY
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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.