Metabolic activity: A novel indicator of neuronal survival in the murine dopaminergic cell line CAD
Apoptosis is implicated in many neurodegenerative diseases, including Parkinson's disease (PD). Neuroprotective strategies targeting apoptosis need to preserve functional integrity of the saved cells to be effective. The aim of the present study was to evaluate a novel approach for analyzing ne...
- Autores:
- Tipo de recurso:
- Fecha de publicación:
- 2005
- Institución:
- Universidad del Rosario
- Repositorio:
- Repositorio EdocUR - U. Rosario
- Idioma:
- eng
- OAI Identifier:
- oai:repository.urosario.edu.co:10336/22406
- Acceso en línea:
- https://doi.org/10.1385/JMN:27:01:65
https://repository.urosario.edu.co/handle/10336/22406
- Palabra clave:
- Biological marker
Carbachol
Caspase inhibitor
Ceramide
Muscarinic receptor
Neurotrophic factor
Neurotrophin 3
Sphingosine derivative
Animal cell
Apoptosis
Article
Brain function
Catecholamine nerve cell
Cell activity
Cell death
Cell function
Cell line
Cell metabolism
Cell survival
Cell viability
Central nervous system
Dopaminergic nerve cell
In vitro study
Metabolic activation
Molecular model
Mouse
Nerve cell
Nonhuman
Parkinson disease
Receptor upregulation
Amino acid chloromethyl ketones
Animals
Apoptosis
Caspases
Cell line
Cell survival
Cysteine proteinase inhibitors
Dopamine
Energy metabolism
Mice
Neurons
Neuroprotective agents
Neurotrophin 3
Sphingosine
Murinae
Cad
Caspase inhibitor
Catecholaminergic cells
Ceramide
Metabolic activity
Microphysiometer
Neuronal apoptosis
Neurotrophin-3
- Rights
- License
- Abierto (Texto Completo)
Summary: | Apoptosis is implicated in many neurodegenerative diseases, including Parkinson's disease (PD). Neuroprotective strategies targeting apoptosis need to preserve functional integrity of the saved cells to be effective. The aim of the present study was to evaluate a novel approach for analyzing neuronal function that monitors cellular metabolic responses to receptor activation using the microphysiometer. N-Acetyl-sphingosine (C2-ceramide) induced cell death of the neuronal cell line, Cath.a-differentiated (CAD) cells, which resemble catecholaminergic cells of the CNS, and provide a useful in vitro model for the cells affected in PD. C2-ceramide also suppressed the metabolic response of CAD cells to muscarinic receptor activation. Pretreatment with the caspase inhibitor Boc-Asp-(OMe)-fluoromethylketone (BAF) plusneurotrophin-3 (NT-3) reduced C2-ceramide-induced CAD cell death, delaying cell death more effectively than either agent alone; and, most significantly, BAF and NT-3 enabled the cells remaining 24 h after toxin treatment to generate a normal metabolic response to the muscarinic agonist carbachol. On the basis of these results, we suggest that measuring metabolic responses to receptor activation is a useful method for following neuronal viability after toxin treatment and that the combination of caspase inhibitors and neurotrophic factors might be a plausible strategy for improving neuronal survival, with critical preservation of metabolic function. Copyright © 2005 Humana Press Inc. All rights of any nature whatsoever reserved. |
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