Evidence map›Paper›PMID 41721218›Full record

ArticleMolecular pain

Top-down descending modulation of dorsal spinal excitatory transmission from the insular cortex.

Qi-Yu Chen, Ren-Hao Liu, Shiwen Xue, Min Zhuo

Abstract read
In one paragraph

Article in Molecular pain. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Qi-Yu ChenInstitute of Neuroscience, Kunming Medical University, Kunming, Yunnan, China.ORCID 0000-0002-5707-6220
Ren-Hao LiuInternational Institute for Brain Research, Qingdao, China.
Shiwen XueInstitute of Neuroscience, Kunming Medical University, Kunming, Yunnan, China.
Min ZhuoInternational Institute for Brain Research, Qingdao, China.ORCID 0000-0001-9062-3241

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The insular cortex (IC), a critical hub for nociception, emotion, and cognition processing, has emerged as a key role in the descending modulation of spinal cord excitability. Although previous studies have suggested that IC may influence spinal nociceptive reflexes through direct or indirect top-down pathways, the specific effects of IC stimulation on spinal nociceptive transmission remain unclear. In this study, by combining in vivo whole-cell patch-clamp, behavioral and morphological approaches, we identified a direct projection from the IC to the contralateral dorsal spinal cord. To determine whether IC activation affect the spinal nociceptive reflex, we measured the spinal nociceptive tail-flick (TF) reflex during IC stimulation. We found that activating the IC by electric stimulation did not significantly alter the spinal TF reflex. Furthermore, in vivo whole-cell patch-clamp recordings from spinal dorsal horn neurons revealed that IC stimulation produced delayed inhibition of spontaneous excitatory transmission in some neurons, while exciting or having no significant effect on others. These results indicate that the top-down modulation from the IC to the spinal cord is not uniformly facilitatory, distinguishing it from the consistently facilitatory effects observed in the anterior cingulate cortex (ACC)-spinal cord projection.

Indexed as

Insular CortexSpinal CordSynaptic TransmissionAnimalsElectric StimulationMalePatch-Clamp TechniquesPosterior Horn CellsRats, Sprague-DawleyReflexdescending facilitationdescending inhibitionInsular cortexpainspinal dorsal horn

Identifiers

PMID41721218
PMCPMC13009838

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.