Presencia de la vía de la fosfatidilinositol-3-quinasa en sinaptosomas de corteza cerebral de rata. Efectos del insulto oxidativo

URANGA, ROMINA; MATEOS, MELINA; GIUSTO, NORMA; SALVADOR, GABRIELA

Mar del Plata, Buenos Aires, Argentina.

Congreso; XIX Reunión Anual de la Sociedad Argentina de Neuroquímica (SAN); 2004

Sociedad Argentina de Neuroquímica

Most of the signal transduction events that regulate neuronal plasticity and central nervous system survival occur in the synapses. In this way, it was demonstrated that oxidative stress induces defects in several synaptic signaling pathways and that this fact is a common mechanism involved in the earlier events of neurodegenerative diseases. Additionaly it has been reported that phosphatidylinositol-3-kinase (PI3K) pathway participates in the molecular mechanisms of several neurodegenerative diseases.The purpose of this work was to identify PI3K pathway in rat cerebral cortex synaptosomes. We used either metabolicaly active synaptosomes or synaptosomes exposed to oxidative stress conditions induced by FeSO4. Western blot assays using antibodies against PI3K regulatory subunit (anti-p85a) led us to identify a protein of approximately 90 kD in both cases. In addition, we were able to determine the presence of Akt  in this experimental model. Glutamate uptake significantly decreased when synaptosomes were exposed to the oxidative injury. Moreover, protein tyrosine phosphorylation was increased in presence of FeSO4. Our results demonstrate that PI3K/Akt pathway is present in isolated synaptic terminals. We can also conclude that glutamate uptake decreases and that tyrosine kinase activity increases under oxidative stress conditions in cerebral cortex synaptosomes.