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Artículo

Calpain-dependent truncated form of TrkB-FL increases in neurodegenerative processes

Danelon, VíctorIcon ; Montroull, Laura EsterIcon ; Unsain, NicolasIcon ; Barker, Philip A.; Masco, Daniel HugoIcon
Fecha de publicación: 09/2016
Editorial: Academic Press Inc Elsevier Science
Revista: Molecular and Cellular Neuroscience
ISSN: 1044-7431
Idioma: Inglés
Tipo de recurso: Artículo publicado
Clasificación temática:
Otras Ciencias Biológicas

Resumen

Recent findings indicate that the mechanisms that drive reshaping of the nervous system are aberrantly activated in epilepsy and several neurodegenerative diseases. The recurrent seizures in epilepsy, particularly in the condition called status epilepticus, can cause permanent neurological damage, resulting in cognitive dysfunction and other serious neurological conditions. In this study, we used an in vitro model of status epilepticus to examine the role of calpain in the degeneration of hippocampal neurons. We grew neurons on a culture system that allowed studying the dendritic and axonal domains separately from the cell bodies. We found that a recently characterized calpain substrate, the neurotrophin receptor TrkB, is cleaved in the dendritic and axonal domain of neurons committed to die, and this constitutes an early step in the neuronal degeneration process. While the full-length TrkB (TrkB-FL) levels decreased, the truncated form of TrkB (Tc TrkB-FL) concurrently increased, leading to a TrkB-FL/Tc TrkB-FL imbalance, which is thought to be causally linked to neurodegeneration. We further show that the treatment with N-acetyl-Leu-Leu-norleucinal, a specific calpain activity blocker, fully protects the neuronal processes from degeneration, prevents the TrkB-FL/Tc TrkB-FL imbalance, and provides full neuroprotection. Moreover, the use of the TrkB antagonist ANA 12 at the time when the levels of TrkB-FL were significantly decreased, totally blocked neuronal death, suggesting that Tc TrkB-FL may have a role in neuronal death. These results indicate that the imbalance of these neurotrophins receptors plays a key role in neurite degeneration induced by seizures.
Palabras clave: Calpain , Neurite Degeneration , Neuronal Death , Status Epilepticus , Trkb-Fl , Truncated Trkb-Fl
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info:eu-repo/semantics/restrictedAccess Excepto donde se diga explícitamente, este item se publica bajo la siguiente descripción: Atribución-NoComercial-SinDerivadas 2.5 Argentina (CC BY-NC-ND 2.5 AR)
Identificadores
URI: http://hdl.handle.net/11336/39600
DOI: http://dx.doi.org/10.1016/j.mcn.2016.07.002
URL: https://www.sciencedirect.com/science/article/pii/S1044743116300768
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Articulos(IIBYT) [569]
Articulos de INSTITUTO DE INVESTIGACIONES BIOLOGICAS Y TECNOLOGICAS
Citación
Danelon, Víctor; Montroull, Laura Ester; Unsain, Nicolas; Barker, Philip A.; Masco, Daniel Hugo; Calpain-dependent truncated form of TrkB-FL increases in neurodegenerative processes; Academic Press Inc Elsevier Science; Molecular and Cellular Neuroscience; 75; 9-2016; 81-92
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