Evidence map›Paper›PMID 23554470›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013

Opposing roles of corticotropin-releasing factor and neuropeptide Y within the dorsolateral bed nucleus of the stria terminalis in the negative affective component of pain in rats.

Soichiro Ide, Taiki Hara, Atsushi Ohno, Ryuta Tamano, Kana Koseki, Tomonori Naka, Chikashi Maruyama, Katsuyuki Kaneda, Mitsuhiro Yoshioka, Masabumi Minami

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
3.5field-weighted citation impact, top 7% 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, 67 citations in OpenAlex.

  1. Article
  2. Neuropeptide Y and Pain: Insights from Brain Research.ACS pharmacology & translational science · 2024
    Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Frontiers in immunology · 2022
    Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
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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

10 authors at 2 institutions in 1 country.

Soichiro IdeDepartment of Pharmacology, Graduate School of Pharmaceutical Sciences, Hokkaido University, Sapporo 060-0812, Japan.
Taiki Hara
Atsushi Ohno
Ryuta Tamano
Kana Koseki
Tomonori Naka
Chikashi Maruyama
Katsuyuki Kaneda
Mitsuhiro Yoshioka
Masabumi Minami
Hokkaido Pharmaceutical University · JPHokkaido University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pain is a complex experience composed of sensory and affective components. Although the neural systems of the sensory component of pain have been studied extensively, those of its affective component remain to be determined. In the present study, we examined the effects of corticotropin-releasing factor (CRF) and neuropeptide Y (NPY) injected into the dorsolateral bed nucleus of the stria terminalis (dlBNST) on pain-induced aversion and nociceptive behaviors in rats to examine the roles of these peptides in affective and sensory components of pain, respectively. In vivo microdialysis showed that formalin-evoked pain enhanced the release of CRF in this brain region. Using a conditioned place aversion (CPA) test, we found that intra-dlBNST injection of a CRF1 or CRF2 receptor antagonist suppressed pain-induced aversion. Intra-dlBNST CRF injection induced CPA even in the absence of pain stimulation. On the other hand, intra-dlBNST NPY injection suppressed pain-induced aversion. Coadministration of NPY inhibited CRF-induced CPA. This inhibitory effect of NPY was blocked by coadministration of a Y1 or Y5 receptor antagonist. Furthermore, whole-cell patch-clamp electrophysiology in dlBNST slices revealed that CRF increased neuronal excitability specifically in type II dlBNST neurons, whereas NPY decreased it in these neurons. Excitatory effects of CRF on type II dlBNST neurons were suppressed by NPY. These results have uncovered some of the neuronal mechanisms underlying the affective component of pain by showing opposing roles of intra-dlBNST CRF and NPY in pain-induced aversion and opposing actions of these peptides on neuronal excitability converging on the same target, type II neurons, within the dlBNST.

Indexed as

Action PotentialsAffective SymptomsAnalysis of VarianceAniline CompoundsAnimalsArginineCorticotropin-Releasing HormoneCyclohexanesDisease Models, AnimalExcitatory Amino Acid AntagonistsFormaldehydeGABA AntagonistsHormone AntagonistsHormonesIn Vitro TechniquesKynurenic Acid2-methyl-4-(N-propyl-N-cycloproanemethylamino)-5-chloro-6-(2,4,6-trichloranilino)pyrimidineAniline Compoundsantisauvagine 30ArginineBIBP 3226Corticotropin-Releasing HormoneCyclohexanesExcitatory Amino Acid AntagonistsFormaldehydeGABA AntagonistsgabazineHormone AntagonistsHormonesKynurenic AcidL 152804Neuropeptide YPeptide FragmentsPyridazinesPyrimidinesXanthenes

Identifiers

PMID23554470
PMCPMC6618927
OpenAlexW1970713268

What OpenQuestion holds

Textmetadata
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.