Activity-induced secretion of semaphorin 3A mediates learning.

AMPA receptors LTP axonal guidance molecules synaptic plasticity

Journal

The European journal of neuroscience
ISSN: 1460-9568
Titre abrégé: Eur J Neurosci
Pays: France
ID NLM: 8918110

Informations de publication

Date de publication:
05 2021
Historique:
revised: 16 03 2021
received: 02 09 2020
accepted: 22 03 2021
pubmed: 28 3 2021
medline: 1 7 2021
entrez: 27 3 2021
Statut: ppublish

Résumé

The semaphorin family is a well-characterized family of secreted or membrane-bound proteins that are involved in activity-independent neurodevelopmental processes, such as axon guidance, cell migration, and immune functions. Although semaphorins have recently been demonstrated to regulate activity-dependent synaptic scaling, their roles in Hebbian synaptic plasticity as well as learning and memory remain poorly understood. Here, using a rodent model, we found that an inhibitory avoidance task, a hippocampus-dependent contextual learning paradigm, increased secretion of semaphorin 3A in the hippocampus. Furthermore, the secreted semaphorin 3A in the hippocampus mediated contextual memory formation likely by driving AMPA receptors into hippocampal synapses via the neuropilin1-plexin A4-semaphorin receptor complex. This signaling process involves alteration of the phosphorylation status of collapsin response mediator protein 2, which has been characterized as a downstream molecule in semaphorin signaling. These findings implicate semaphorin family as a regulator of Hebbian synaptic plasticity and learning.

Identifiants

pubmed: 33772906
doi: 10.1111/ejn.15210
pmc: PMC8252788
doi:

Substances chimiques

Semaphorin-3A 0
Semaphorins 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

3279-3293

Informations de copyright

© 2021 The Authors. European Journal of Neuroscience published by Federation of European Neuroscience Societies and John Wiley & Sons Ltd.

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Auteurs

Aoi Jitsuki-Takahashi (A)

Department of Physiology, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
Department of Molecular Pharmacology and Neurobiology, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
Department of Biochemistry, Tokyo Women's Medical University School of Medicine, Tokyo, Japan.

Susumu Jitsuki (S)

Department of Physiology, Yokohama City University Graduate School of Medicine, Yokohama, Japan.

Naoya Yamashita (N)

Department of Pharmacology, Juntendo University School of Medicine, Tokyo, Japan.

Meiko Kawamura (M)

Department of Animal Model Development, Brain Research Institute, Niigata University, Niigata, Japan.

Manabu Abe (M)

Department of Animal Model Development, Brain Research Institute, Niigata University, Niigata, Japan.

Kenji Sakimura (K)

Department of Animal Model Development, Brain Research Institute, Niigata University, Niigata, Japan.

Akane Sano (A)

Department of Physiology, Yokohama City University Graduate School of Medicine, Yokohama, Japan.

Fumio Nakamura (F)

Department of Biochemistry, Tokyo Women's Medical University School of Medicine, Tokyo, Japan.

Yoshio Goshima (Y)

Department of Molecular Pharmacology and Neurobiology, Yokohama City University Graduate School of Medicine, Yokohama, Japan.

Takuya Takahashi (T)

Department of Physiology, Yokohama City University Graduate School of Medicine, Yokohama, Japan.

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Classifications MeSH