Evidence map›Paper›PMID 27551099›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2016

Reassessment of long-term depression in cerebellar Purkinje cells in mice carrying mutated GluA2 C terminus.

Kazuhiko Yamaguchi, Shigeyoshi Itohara, Masao Ito

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

22 citing papers in PubMed, 45 citations in OpenAlex.

  1. Consensus Paper: Models of Cerebellar Functions.Cerebellum (London, England) · 2026
    Review
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  5. Unraveling the mysteries of dendritic spine dynamics: Five key principles shaping memory and cognition.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2023
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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

3 authors at 1 institution in 1 country.

Kazuhiko YamaguchiLaboratory for Behavioral Genetics, RIKEN Brain Science Institute, Wako, Saitama 353-0198, Japan;
Shigeyoshi ItoharaLaboratory for Behavioral Genetics, RIKEN Brain Science Institute, Wako, Saitama 353-0198, Japan;
Masao ItoSenior Advisor's Office, RIKEN Brain Science Institute, Wako, Saitama 353-0198, Japan masao@brain.riken.jp.
RIKEN Center for Brain Science · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Long-term depression (LTD) of synaptic transmission from parallel fibers (PFs) to a Purkinje cell (PC) in the cerebellum has been considered to be a core mechanism of motor learning. Recently, however, discrepancies between LTD and motor learning have been reported in mice with a mutation that targeted the expression of PF-PC LTD by blocking AMPA-subtype glutamate receptor internalization regulated via the phosphorylation of AMPA receptors. In these mice, motor learning behavior was normal, but no PF-PC LTD was observed. We reexamined slices obtained from these GluA2 K882A and GluA2 Δ7 knockin mutants at 3-6 mo of age. The conventional protocols of stimulation did not induce LTD in these mutant mice, as previously reported, but surprisingly, LTD was induced using certain modified protocols. Such modifications involved increases in the number of PF stimulation (from one to two or five), replacement of climbing fiber stimulation with somatic depolarization (50 ms), filling a patch pipette with a Cs(+)-based solution, or extension of the duration of conjunction. We also found that intracellular infusion of a selective PKCα inhibitor (Gö6976) blocked LTD induction in the mutants, as in WT, suggesting that functional compensation occurred downstream of PKCα. The possibility that LTD in the mutants was caused by changes in membrane resistance, access resistance, or presynaptic property was excluded. The present results demonstrate that LTD is inducible by intensified conjunctive stimulations even in K882A and Δ7 mutants, indicating no contradiction against the LTD hypothesis of motor learning.

Indexed as

MutationAnimalsCarbazolesLearningLong-Term Synaptic DepressionMiceMice, TransgenicMotor ActivityPatch-Clamp TechniquesPhosphorylationProtein Kinase C-alphaProtein Kinase InhibitorsPurkinje CellsReceptors, AMPASynapsesSynaptic TransmissionCarbazolesglutamate receptor ionotropic, AMPA 2Go 6976Prkca protein, mouseProtein Kinase C-alphaProtein Kinase InhibitorsReceptors, AMPAcerebellumLTDMarr–Albus–Ito hypothesismotor-learningslice

Identifiers

PMID27551099
PMCPMC5018784
OpenAlexW2513610447

What OpenQuestion holds

Textmetadata
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.