Evidence map›Paper›PMID 26888105›Full record

ArticleJournal of neurophysiology2016

Synaptic and network consequences of monosynaptic nociceptive inputs of parabrachial nucleus origin in the central amygdala.

Yae K Sugimura, Yukari Takahashi, Ayako M Watabe, Fusao Kato

Open access · greenAbstract read
In one paragraph

Article in Journal of neurophysiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
5.1field-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

40 citing papers in PubMed, 63 citations in OpenAlex.

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  10. The parabrachial to central amygdala pathway is critical to injury-induced pain sensitization in mice.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 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

4 authors at 1 institution in 1 country.

Yae K SugimuraDepartment of Neuroscience, The Jikei University School of Medicine, Minato, Tokyo, Japan; Center for Neuroscience of Pain, The Jikei University School of Medicine, Minato, Tokyo, Japan; Research Fellow of Japan Society for the Promotion of Science, Tokyo, Japan;
Yukari TakahashiDepartment of Neuroscience, The Jikei University School of Medicine, Minato, Tokyo, Japan; Center for Neuroscience of Pain, The Jikei University School of Medicine, Minato, Tokyo, Japan;
Ayako M WatabeDepartment of Neuroscience, The Jikei University School of Medicine, Minato, Tokyo, Japan; Center for Neuroscience of Pain, The Jikei University School of Medicine, Minato, Tokyo, Japan; Precursory Research for Embryonic Science and Technology, Japan Science and Technology Agency, Kawaguchi, Saitama, Japan; and Nagoya University Graduate School of Medicine, Nagoya, Japan.
Fusao KatoDepartment of Neuroscience, The Jikei University School of Medicine, Minato, Tokyo, Japan; Center for Neuroscience of Pain, The Jikei University School of Medicine, Minato, Tokyo, Japan; Nagoya University Graduate School of Medicine, Nagoya, Japan fusao@jikei.ac.jp.ORCID 0000-0003-0031-9946
Jikei University School of Medicine · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A large majority of neurons in the superficial layer of the dorsal horn projects to the lateral parabrachial nucleus (LPB). LPB neurons then project to the capsular part of the central amygdala (CeA; CeC), a key structure underlying the nociception-emotion link. LPB-CeC synaptic transmission is enhanced in various pain models by using electrical stimulation of putative fibers of LPB origin in brain slices. However, this approach has limitations for examining direct monosynaptic connections devoid of directly stimulating fibers from other structures and local GABAergic neurons. To overcome these limitations, we infected the LPB of rats with an adeno-associated virus vector expressing channelrhodopsin-2 and prepared coronal and horizontal brain slices containing the amygdala. We found that blue light stimulation resulted in monosynaptic excitatory postsynaptic currents (EPSCs), with very small latency fluctuations, followed by a large polysynaptic inhibitory postsynaptic current in CeC neurons, regardless of the firing pattern type. Intraplantar formalin injection at 24 h before slice preparation significantly increased EPSC amplitude in late firing-type CeC neurons. These results indicate that direct monosynaptic glutamatergic inputs from the LPB not only excite CeC neurons but also regulate CeA network signaling through robust feed-forward inhibition, which is under plastic modulation in response to persistent inflammatory pain.

Indexed as

Action PotentialsAnimalsCentral Amygdaloid NucleusDisease Models, AnimalExcitatory Postsynaptic PotentialsGlutamic AcidInhibitory Postsynaptic PotentialsMaleNeural PathwaysNeuronal PlasticityNeuronsNociceptive PainParabrachial NucleusRats, WistarSynapsesTissue Culture TechniquesGlutamic Acidchannelrhodopsin-2excitatory postsynaptic currentfeed-forward inhibitionpainrat

Identifiers

PMID26888105
PMCPMC4922599
OpenAlexW2278798383

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.