CHANGES IN GLUTAMATERGIC NMDA RECEPTOR SUBUNITS BY ENDOBAIN E, AN ENDOGENOUS Na+, K+-ATPase INHIBITOR

M. G. BERSIER; C. PEÑA; G. RODRÍGUEZ DE LORES ARNAIZ

Portland, Oregon, EE.UU.

Congreso; XXXVII Congreso de la Sociedad Americana de Neuroquímica (ASN), Portland, Oregon, EE.UU.; 2006

Sociedad Americana de Neuroquímica (ASN)

Endobain E is a soluble brain factor isolated from cerebral cortex which shares biological properties with ouabain, one of them is the inhibition of Na+, K+-ATPase activity. In previous studies carried out in this laboratory, the ability of endobain E to decrease [3H]dizocilpine binding to glutamatergic ionotropic NMDA receptor was described. In the search of an interplay between NMDA receptor and Na+, K+-ATPase, herein we analyzed the expression of NMDA subunits after endobain E treatment. Wistar rats were administered i.c.v. stereotaxically with endobain E or saline (control) solutions; 3 days later animals were decapitated, cerebral cortex and hippocampus removed and tissues were subjected to differential centrifugation to isolate crude membrane fractions. Western blot analysis was performed, and the antibodies against subunists NR1, NR2A and NR2B of NMDA receptor were employed. The bands were visualized by quimiluminscence. Expression of NR1, the most abundant subunit, highly increased in cerebral cortex and hippocampus after endobain E administration. NR2A expression resulted enhanced in cerebral cortex but diminished in hippocampus. NR2B, the less abundant subunit, remained unaltered by the treatment. Results indicate that endobain E produced differential modifications in the expression of NMDA receptor subunits, supporting the hypothesis of a relationship between the glutamatergic ionotropic NMDA receptor and Na+, K+-ATPase.