Apoptosis of glutamatergic neurons fails to trigger a neurogenic response in the adult neocortex.

Imagen de Frank Diaz
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TítuloApoptosis of glutamatergic neurons fails to trigger a neurogenic response in the adult neocortex.
Publication TypeJournal Article
Year of Publication2013
AutoresDiaz, F, McKeehan, N, Kang, W, Hébert, JM
JournalJ Neurosci
Volume33
Issue15
Pagination6278-84
Date Published2013 Apr 10
ISSN1529-2401
Palabras claveAnimals, Apoptosis, Basic Helix-Loop-Helix Transcription Factors, Caspase 8, Diphtheria Toxin, Glutamates, Mice, Mice, Transgenic, Microglia, Microtubule-Associated Proteins, Neocortex, Nerve Degeneration, Nerve Tissue Proteins, Neurogenesis, Neurons, Neuropeptides, Up-Regulation
Abstract

Adult neurogenesis is actively studied in part because of the potential to manipulate endogenous neural stem and progenitor cells for tissue repair. Although constitutive generation of neurons in the adult rodent olfactory bulb and hippocampal dentate gyrus is widely accepted and stroke-induced generation of striatal inhibitory neurons consistently observed, evidence supporting the generation of neurons in the neocortex after neuronal loss remains slim. Nevertheless, a few studies suggested that targeted apoptosis of neocortical glutamatergic neurons could trigger the generation of new ones in the adult brain. In light of such studies, we tested whether apoptosis of glutamatergic cortical neurons using two novel transgenic approaches in mice, an inducible Caspase-8 protein and an inducible diphtheria toxin gene, results in new neurons. After a thorough analysis, no new neurons were detected in the neocortex. Interestingly, an increase in the expression of the neuroblast marker DCX was observed in both models, in some cases in cells with morphologies previously associated with poststroke neuroblasts, but DCX(+) cells coexpressed the oligodendrocyte precursor marker Olig2, suggesting caution when using DCX as a marker for neuroblasts after injury. Given that the adult neocortex lacks an innate potential to regenerate lost glutamatergic neurons, future strategies should concentrate on manipulating the differentiation potential of endogenous or exogenous precursor cells.

DOI10.1523/JNEUROSCI.5885-12.2013
Alternate JournalJ. Neurosci.
PubMed ID23575827
PubMed Central IDPMC3644398
Grant ListF31 NS052932 / NS / NINDS NIH HHS / United States
MH070596 / MH / NIMH NIH HHS / United States
NS073761 / NS / NINDS NIH HHS / United States
R21 NS073761 / NS / NINDS NIH HHS / United States
T32 GM007288 / GM / NIGMS NIH HHS / United States