Evidence map›Paper›PMID 23077049›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2012

Serotonin-induced cleavage of the atypical protein kinase C Apl III in Aplysia.

Joanna K Bougie, Diancai Cai, Margaret Hastings, Carole A Farah, Shanping Chen, Xiaotang Fan, Patrick K McCamphill, David L Glanzman, Wayne S Sossin

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing 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

29 citing papers in PubMed, 44 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. Article
  6. Isoform Specificity of PKMs during Long-Term Facilitation inThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Article
  7. Review
  8. Review
  9. Article
  10. PAR3-PAR6-atypical PKC polarity complex proteins in neuronal polarization.Cellular and molecular life sciences : CMLS · 2018
    Review
  11. Review
  12. Review
  13. Article
  14. 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
  15. Article
  16. Article
  17. Article
  18. Article
  19. The Role of Functional Prion-Like Proteins in the Persistence of Memory.Cold Spring Harbor perspectives in biology · 2016
    Review
  20. 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

9 authors at 3 institutions in 3 countries.

Joanna K BougieDepartment of Psychology, McGill University, Montreal Neurological Institute, Montreal, Quebec H3A 1B1, Canada.
Diancai Cai
Margaret Hastings
Carole A Farah
Shanping Chen
Xiaotang Fan
Patrick K McCamphill
David L Glanzman
Wayne S Sossin
McGill University · CAUniversity of California, Los Angeles · USMontreal Neurological Institute and Hospital · CA

Funding

Hebbian Long-Term Potentiation and Learning in AplysiaR37NS029563 · NINDS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI GLANZMAN, DAVID L · 2005 to 2011
$2.9M
Mechanisms of Long-Term Memory Maintenance in Aplysia.R01MH096120 · NIMH · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI GLANZMAN, DAVID L · 2012 to 2016
$1.9M
CIHR MOP 12046NIMH NIH HHS R01 MH096120NINDS NIH HHS R37 NS029563
6 · The paper itself

Abstract

A constitutively active kinase, known as protein kinase Mζ (PKMζ), is proposed to act as a long-lasting molecular memory trace. While PKMζ is formed in rodents through translation of a transcript initiating in an intron of the protein kinase Cζ (PKCζ) gene, this transcript does not exist in Aplysia californica despite the fact that inhibitors of PKMζ erase memory in Aplysia in a fashion similar to rodents. We have previously shown that, in Aplysia, the ortholog of PKCζ, PKC Apl III, is cleaved by calpain to form a PKM after overexpression of PKC Apl III. We now show that kinase activity is required for this cleavage. We further use a FRET reporter to measure cleavage of PKC Apl III into PKM Apl III in live neurons using a stimulus that induces plasticity. Our results show that a 10 min application of serotonin induces cleavage of PKC Apl III in motor neuron processes in a calpain- and protein synthesis-dependent manner, but does not induce cleavage of PKC Apl III in sensory neuron processes. Furthermore, a dominant-negative PKM Apl III expressed in the motor neuron blocked the late phase of intermediate-term facilitation in sensory-motor neuron cocultures induced by 10 min of serotonin. In summary, we provide evidence that PKC Apl III is cleaved into PKM Apl III during memory formation, that the requirements for cleavage are the same as the requirements for the plasticity, and that PKM in the motor neuron is required for intermediate-term facilitation.

Indexed as

AnimalsAplysiaCell LineCells, CulturedIsoenzymesMemoryMotor NeuronsProtein Kinase CProtein Kinase C zetaSerotoninIsoenzymesProtein Kinase CProtein Kinase C zetaSerotonin

Identifiers

PMID23077049
PMCPMC6621423
OpenAlexW2059927418

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.