Evidence map›Paper›PMID 28905207›Full record

ArticlePsychopharmacology2017

Role of vasopressin V1a receptor in ∆

Nobuaki Egashira, Emi Koushi, Takayuki Myose, Akito Tanoue, Kenichi Mishima, Ryota Tsuchihashi, Junei Kinjo, Hiroyuki Tanaka, Satoshi Morimoto, Katsunori Iwasaki

Abstract read
PubMed Publisher
In one paragraph

Article in Psychopharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact, top 88% 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

1 citing paper in PubMed, 2 citations in OpenAlex.

  1. Review
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 4 institutions in 1 country.

Nobuaki EgashiraDepartment of Neuropharmacology, Faculty of Pharmaceutical Sciences, Fukuoka University, 8-19-1 Nanakuma, Jonan-ku, Fukuoka, 814-0180, Japan. n-Egashi@Pharm.Med.Kyushu-u.Ac.Jp.
Emi KoushiDepartment of Neuropharmacology, Faculty of Pharmaceutical Sciences, Fukuoka University, 8-19-1 Nanakuma, Jonan-ku, Fukuoka, 814-0180, Japan.
Takayuki MyoseDepartment of Pharmacology, Faculty of Pharmaceutical Sciences, Fukuoka University, 8-19-1 Nanakuma, Jonan-ku, Fukuoka, 814-0180, Japan.
Akito TanoueDepartment of Pharmacology, National Research Institute for Child Health and Development, 2-10-1 Okura, Setagaya-ku, Tokyo, 157-8535, Japan.
Kenichi MishimaDepartment of Pharmacology, Faculty of Pharmaceutical Sciences, Fukuoka University, 8-19-1 Nanakuma, Jonan-ku, Fukuoka, 814-0180, Japan.
Ryota TsuchihashiDepartment of Pharmacognosy, Faculty of Pharmaceutical Sciences, Fukuoka University, 8-19-1 Nanakuma, Jonan-ku, Fukuoka, 814-0180, Japan.
Junei KinjoDepartment of Pharmacognosy, Faculty of Pharmaceutical Sciences, Fukuoka University, 8-19-1 Nanakuma, Jonan-ku, Fukuoka, 814-0180, Japan.
Hiroyuki TanakaDepartment of Pharmacognosy, Graduate School of Pharmaceutical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka, 812-8582, Japan.
Satoshi MorimotoDepartment of Pharmacognosy, Graduate School of Pharmaceutical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka, 812-8582, Japan.
Katsunori IwasakiDepartment of Neuropharmacology, Faculty of Pharmaceutical Sciences, Fukuoka University, 8-19-1 Nanakuma, Jonan-ku, Fukuoka, 814-0180, Japan.
Fukuoka University · JPKyushu University · JPKyushu University Hospital · JPNational Center For Child Health and Development · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

rationaleCannabis is a widely used illicit substance. ∆

objectivesThe present study was designed to examine the possible involvement of V1a and V1b receptors in THC-induced catalepsy-like immobilization.

methodsThe induction of catalepsy following treatment with THC (10 mg/kg, i.p.) or haloperidol (1 mg/kg, i.p.) was evaluated in wild-type (WT), V1a receptor knockout (V1aRKO), and V1b receptor knockout (V1bRKO) mice. The effect of treatment with the selective 5-hydroxytryptamine

resultsTHC and haloperidol markedly caused catalepsy in V1bRKO mice as well as in WT mice. However, V1aRKO mice exhibited a reduction in catalepsy induced by THC but not by haloperidol. WAY100635 dramatically enhanced THC-induced catalepsy in V1aRKO mice. Although VMAX-357 (10 mg/kg, p.o.) but not ORG-52186 significantly attenuated THC-induced catalepsy, it had no significant effect on the enhancement of THC-induced catalepsy by WAY100635 in ddY mice.

conclusionsThese findings suggest that V1a receptor regulates THC-induced catalepsy-like immobilization.

Indexed as

AnimalsCannabinoid Receptor AgonistsCannabinoidsCatalepsyDose-Response Relationship, DrugDronabinolHaloperidolImmobilizationMaleMiceMice, Inbred C57BLMice, KnockoutRandom AllocationReceptors, VasopressinAVPR1A protein, humanCannabinoid Receptor AgonistsCannabinoidsDronabinolHaloperidolReceptors, Vasopressin∆9-TetrahydrocannabinolCatalepsyV1a receptorV1b receptorVasopressin

Identifiers

PMID28905207
OpenAlexW2754675059

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.