Evidence map›Paper›PMID 26807827›Full record

ArticlePloS one2016

Caspr3-Deficient Mice Exhibit Low Motor Learning during the Early Phase of the Accelerated Rotarod Task.

Haruna Hirata, Aki Takahashi, Yasushi Shimoda, Tsuyoshi Koide

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

17 citing papers in PubMed, 36 citations in OpenAlex.

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  7. Bmal1 Modulates Striatal cAMP Signaling and Motor Learning.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
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  12. Postnatal Sox6 Regulates Synaptic Function of Cortical Parvalbumin-Expressing Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
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  15. The efficacy of combination treatment of gabapentin and electro-acupuncture on paclitaxel-induced neuropathic pain.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2017
    Article
  16. Review
  17. 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

4 authors at 3 institutions in 1 country.

Haruna HirataDepartment of Bioengineering, Nagaoka University of Technology, Nagaoka, Niigata, 940-2188, Japan.
Aki TakahashiMouse Genomics Resource Laboratory, National Institute of Genetics (NIG), Mishima, Shizuoka, 411-8540, Japan.
Yasushi ShimodaDepartment of Bioengineering, Nagaoka University of Technology, Nagaoka, Niigata, 940-2188, Japan.
Tsuyoshi KoideMouse Genomics Resource Laboratory, National Institute of Genetics (NIG), Mishima, Shizuoka, 411-8540, Japan.
Nagaoka University of Technology · JPResearch Organization of Information and Systems · JPThe Graduate University for Advanced Studies, SOKENDAI · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Caspr3 (Contactin-associated protein-like 3, Cntnap3) is a neural cell adhesion molecule belonging to the Caspr family. We have recently shown that Caspr3 is expressed abundantly between the first and second postnatal weeks in the mouse basal ganglia, including the striatum, external segment of the globus pallidus, subthalamic nucleus, and substantia nigra. However, its physiological role remains largely unknown. In this study, we conducted a series of behavioral analyses on Capsr3-knockout (KO) mice and equivalent wild-type (WT) mice to investigate the role of Caspr3 in brain function. No significant differences were observed in most behavioral traits between Caspr3-KO and WT mice, but we found that Caspr3-KO mice performed poorly during the early phase of the accelerated rotarod task in which latency to falling off a rod rotating with increasing velocity was examined. In the late phase, the performance of the Caspr3-KO mice caught up to the level of WT mice, suggesting that the deletion of Caspr3 caused a delay in motor learning. We then examined changes in neural activity after training on the accelerated rotarod by conducting immunohistochemistry using antibody to c-Fos, an indirect marker for neuronal activity. Experience of the accelerated rotarod task caused increases in the number of c-Fos-positive cells in the dorsal striatum, cerebellum, and motor cortex in both Caspr3-KO and WT mice, but the number of c-Fos-positive cells was significantly lower in the dorsal striatum of Caspr3-KO mice than in that of WT mice. The expression of c-Fos in the ventral striatum of Caspr3-KO and WT mice was not altered by the training. Our findings suggest that reduced activation of neural cells in the dorsal striatum in Caspr3-KO mice leads to a decline in motor learning in the accelerated rotarod task.

Indexed as

AnimalsCerebellumCorpus StriatumLearningMaleMembrane ProteinsMiceMice, KnockoutMotor CortexMotor SkillsNerve Tissue ProteinsNeuronsProto-Oncogene Proteins c-fosRotarod Performance TestCaspr3 protein, mouseMembrane ProteinsNerve Tissue ProteinsProto-Oncogene Proteins c-fos

Identifiers

PMID26807827
PMCPMC4726695
OpenAlexW2411552635

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.