Evidence map›Paper›PMID 27980071›Full record

ArticleLearning & memory (Cold Spring Harbor, N.Y.)2017

A PKM generated by calpain cleavage of a classical PKC is required for activity-dependent intermediate-term facilitation in the presynaptic sensory neuron of Aplysia.

Carole A Farah, Margaret H Hastings, Tyler W Dunn, Katrina Gong, Danay Baker-Andresen, Wayne S Sossin

Open access · diamondAbstract read
In one paragraph

Article in Learning & memory (Cold Spring Harbor, N.Y.), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
–field-weighted citation impact
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

13 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. The Roles of Par3, Par6, and aPKC Polarity Proteins in Normal Neurodevelopment and in Neurodegenerative and Neuropsychiatric Disorders.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
    Review
  3. Article
  4. Article
  5. Isoform Specificity of PKMs during Long-Term Facilitation inThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Article
  6. Review
  7. On the cause of sleep: Protein fragments, the concept of sentinels, and links to epilepsy.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  8. Anterograde and retrograde signaling by anProceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  9. Review
  10. Review
  11. Article
  12. Cell-Specific PKM Isoforms Contribute to the Maintenance of Different Forms of Persistent Long-Term Synaptic Plasticity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017
    Article
  13. 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

6 authors at 2 institutions in 1 country.

Carole A FarahDepartment of Neurology and Neurosurgery, Montreal Neurological Institute, McGill University, Montreal, Quebec H3A 2B4, Canada.
Margaret H HastingsDepartment of Psychology, McGill University, Montreal Neurological Institute, Montreal, Quebec H3A 1B1, Canada.
Tyler W DunnDepartment of Neurology and Neurosurgery, Montreal Neurological Institute, McGill University, Montreal, Quebec H3A 2B4, Canada.
Katrina GongDepartment of Neurology and Neurosurgery, Montreal Neurological Institute, McGill University, Montreal, Quebec H3A 2B4, Canada.
Danay Baker-AndresenDepartment of Neurology and Neurosurgery, Montreal Neurological Institute, McGill University, Montreal, Quebec H3A 2B4, Canada.
Wayne S SossinDepartment of Neurology and Neurosurgery, Montreal Neurological Institute, McGill University, Montreal, Quebec H3A 2B4, Canada wayne.sossin@mcgill.ca.
McGill University · CAMontreal Neurological Institute and Hospital · CA

Funding

CIHR MOP 12046CIHR MOP 340328
6 · The paper itself

Abstract

Atypical PKM, a persistently active form of atypical PKC, is proposed to be a molecular memory trace, but there have been few examinations of the role of PKMs generated from other PKCs. We demonstrate that inhibitors used to inhibit PKMs generated from atypical PKCs are also effective inhibitors of other PKMs. In contrast, we demonstrate that dominant-negative PKMs show isoform-specificity. A dominant-negative PKM from the classical PKC Apl I blocks activity-dependent intermediate-term facilitation (a-ITF) when expressed in the sensory neuron, while a dominant-negative PKM from the atypical PKC Apl III does not. Consistent with a specific role for PKM Apl I in activity-dependent facilitation, live imaging FRET-based cleavage assays reveal that activity leads to cleavage of the classical PKC Apl I, but not the atypical PKC Apl III in the sensory neuron varicosities of Aplysia In contrast, massed intermediate facilitation (m-ITF) induced by 10 min of 5HT is sufficient for cleavage of the atypical PKC Apl III in the motor neuron. Interestingly, both cleavage of PKC Apl I in the sensory neuron during a-ITF and cleavage of PKC Apl III in the motor neuron during m-ITF are inhibited by a dominant-negative form of a penta-EF hand containing classical calpain cloned from Aplysia Consistent with a role for PKMs in plasticity, this dominant-negative calpain also blocks both a-ITF when expressed in the sensory neuron and m-ITF when expressed in the motor neuron. This study broadens the role of PKMs in synaptic plasticity in two significant ways: (i) PKMs generated from multiple isoforms of PKC, including classical isoforms, maintain memory traces; (ii) PKMs play roles in the presynaptic neuron.

Indexed as

AnimalsAplysiaBenzophenanthridinesCalpainCells, CulturedEnzyme InhibitorsFluorescence Resonance Energy TransferGene Expression RegulationMembrane PotentialsMicroinjectionsMotor NeuronsNervous SystemNeuronal PlasticityPotassium ChloridePresynaptic TerminalsProtein IsoformsBenzophenanthridinesCalpainchelerythrineEnzyme InhibitorsPotassium ChlorideProtein IsoformsProtein Kinase CSerotonin

Identifiers

PMID27980071
PMCPMC5159657
OpenAlexW2564493753

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.