Brain-derived neurotrophic factor mediates neuroprotection against Aß-induced toxicity through a mechanism independent on adenosine 2A receptor activation.
Growth Factors
; 33(4): 298-308, 2015.
Article
em En
| MEDLINE
| ID: mdl-26365294
ABSTRACT
Brain-derived neurotrophic factor (BDNF) promotes neuronal survival through TrkB-FL activation. The activation of adenosine A2A receptors (A2AR) is essential for most of BDNF-mediated synaptic actions, such as synaptic plasticity, transmission and neurotransmitter release. We now aimed at evaluating the A2AR influence upon BDNF-mediated neuroprotection against Aß25-35 toxicity in cultured neurons. Results showed that BDNF increases cell survival and reduces the caspase-3 and calpain activation induced by amyloid-ß (Aß) peptide, in a mechanism probably dependent on PLCγ pathway. This BDNF-mediated neuroprotection is not affected by A2AR activation or inhibition. Moreover neither activation nor inhibition of A2AR, per se, significantly influenced Aß-induced neuronal death on calpain-mediated cleavage of TrkB induced by Aß. In conclusion, these results suggest that, in opposition to the fast synaptic actions of BDNF, the neuroprotective actions of this neurotrophin against a strong Aß insult do not require the activation of A2AR.
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Texto completo:
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Fármacos Neuroprotetores
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Fator Neurotrófico Derivado do Encéfalo
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Receptores A2 de Adenosina
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Neurônios
Limite:
Animals
Idioma:
En
Ano de publicação:
2015
Tipo de documento:
Article