Age-related changes in layer II immature neurons of the murine piriform cortex.

aging brain plasticity cerebral cortex mice neurogenesis piriform cortex

Journal

Frontiers in cellular neuroscience
ISSN: 1662-5102
Titre abrégé: Front Cell Neurosci
Pays: Switzerland
ID NLM: 101477935

Informations de publication

Date de publication:
2023
Historique:
received: 13 04 2023
accepted: 14 07 2023
medline: 14 8 2023
pubmed: 14 8 2023
entrez: 14 8 2023
Statut: epublish

Résumé

The recent identification of a population of non-newly born, prenatally generated "immature" neurons in the layer II of the piriform cortex (cortical immature neurons, cINs), raises questions concerning their maintenance or depletion through the lifespan. Most forms of brain structural plasticity progressively decline with age, a feature that is particularly prominent in adult neurogenesis, due to stem cell depletion. By contrast, the entire population of the cINs is produced during embryogenesis. Then these cells simply retain immaturity in postnatal and adult stages, until they "awake" to complete their maturation and ultimately integrate into neural circuits. Hence, the question remains open whether the cINs, which are not dependent on stem cell division, might follow a similar pattern of age-related reduction, or in alternative, might leave a reservoir of young, undifferentiated cells in the adult and aging brain. Here, the number and features of cINs were analyzed in the mouse piriform cortex from postnatal to advanced ages, by using immunocytochemistry for the cytoskeletal marker doublecortin. The abundance and stage of maturation of cINs, along with the expression of other markers of maturity/immaturity were investigated. Despite a marked decrease in this neuronal population during juvenile stages, reminiscent of that observed in hippocampal neurogenesis, a small amount of highly immature cINs persisted up to advanced ages. Overall, albeit reducing in number with increasing age, we report that the cINs are present through the entire animal lifespan.

Identifiants

pubmed: 37576566
doi: 10.3389/fncel.2023.1205173
pmc: PMC10416627
doi:

Types de publication

Journal Article

Langues

eng

Pagination

1205173

Informations de copyright

Copyright © 2023 Ghibaudi, Marchetti, Vergnano, La Rosa, Benedetti, Couillard-Despres, Farioli-Vecchioli and Bonfanti.

Déclaration de conflit d'intérêts

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

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Auteurs

Marco Ghibaudi (M)

Neuroscience Institute Cavalieri Ottolenghi (NICO), Orbassano, Italy.
Department of Veterinary Sciences, University of Turin, Turin, Italy.

Nicole Marchetti (N)

Institute of Biochemistry and Cell Biology, National Research Council, Rome, Italy.

Elena Vergnano (E)

Neuroscience Institute Cavalieri Ottolenghi (NICO), Orbassano, Italy.

Chiara La Rosa (C)

Neuroscience Institute Cavalieri Ottolenghi (NICO), Orbassano, Italy.

Bruno Benedetti (B)

Institute of Experimental Neuroregeneration, Paracelsus Medical University, Salzburg, Austria.
Spinal Cord Injury and Tissue Regeneration Center Salzburg (SCI-TReCS), Salzburg, Austria.
Austrian Cluster for Tissue Regeneration, Vienna, Austria.

Sebastien Couillard-Despres (S)

Institute of Experimental Neuroregeneration, Paracelsus Medical University, Salzburg, Austria.
Spinal Cord Injury and Tissue Regeneration Center Salzburg (SCI-TReCS), Salzburg, Austria.
Austrian Cluster for Tissue Regeneration, Vienna, Austria.

Stefano Farioli-Vecchioli (S)

Institute of Biochemistry and Cell Biology, National Research Council, Rome, Italy.

Luca Bonfanti (L)

Neuroscience Institute Cavalieri Ottolenghi (NICO), Orbassano, Italy.
Department of Veterinary Sciences, University of Turin, Turin, Italy.

Classifications MeSH