MODULATION OF NMDA RECEPTOR SUBUNIT EXPRESSION BY ADMINISTRATION OF A Na+, K+-ATPase INHIBITOR

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

Córdoba

Congreso; XXXVIII Reunión Anual de la Asociación Argentina de Farmacología Experimental (SAFE); 2006

Asociación Argentina de Farmacología Experimental (SAFE)

Endobain E is a soluble brain factor isolated from cerebral cortex which shares biological properties with ouabain, including the inhibition of Na+, K+-ATPase activity. Endobain E decreases [3H] dizocilpine binding to NMDA receptor. 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. Endobain E was isolated by gel filtration and anionic exchange HPLC from a rat brain soluble fraction. Rats were administered i.c.v. with endobain E or saline solutions; 3 days later, animals were decapitated, cerebral cortex and hippocampus removed and crude membrane fractions isolated. NR1, NR2A, NR2B and NR2C subunits were quantified by Western blot. Results were expressed as the ratio between treated versus control. After administration of 10 ml endobain E (1 ml = 28 mg tissue) NR1 expression enhanced 5 fold and 2.5 fold in cerebral cortex and hippocampus, respectively. NR2A expression increased 2 fold in cerebral cortex and 1.5 fold in hippocampus. NR2B expression rised 3 fold in cerebral cortex but remained unaltered in hippocampus. NR2C expression was unaffected in either area. Lower changes were found with 1 ml of endobain E. Results indicate that endogenous Na+, K+-ATPase inhibitor endobain E modifies the expression of NMDA receptor subunits, supporting the hypothesis of a relationship between this receptor and Na+, K+-ATPase at synaptic region.