We found a match
Your institution may have rights to this item. Sign in to continue.
- Title
Glutamate modulates sodium-potassium-ATPase through cyclic GMP and cyclic GMP-dependent protein kinase in rat striatum.
- Authors
Munhoz, Carolina Demarchi; Kawamoto, Elisa Mitiko; de Sá Lima, Larissa; Lepsch, Lucilia Brochado; Glezer, Isaias; Marcourakis, Tania; Scavone, Cristoforo
- Abstract
Excessive excitatory action of glutamate and nitric oxide (NO) has been implicated in degeneration of striatal neurons. Evidence had been provided that Na+K+-ATPase might be involved in this process. Here we investigated whether glutamate-regulated messengers, such as NO and cyclic GMP, could modulate the activity of membrane Na+K+-ATPase. Our results demonstrated that NO donors sodium nitroprusside (SNP at 30 and 300 μ M) and S-nitroso-N-acetylpenicillamine (SNAP at 200 μ M) increased α2,3Na+K+-ATPase activity which was blocked by the NO chelator, haemoglobin and was independent of [Na+]. This regulation was associated with cGMP synthesis and mimicked by glutamate (300 μ M) and 8-Br-cyclic GMP (4 m M). 8-Br-cGMP-induced stimulation of Na+K+-ATPase activity could be blocked by KT5823 (an inhibitor of cGMP-dependent protein kinase, PKG), but not by KT5720 (an inhibitor of cAMP-dependent protein kinase, PKA). N-Methyl- D-aspartate (NMDA) receptors appeared to be involved in the effect of glutamate, since MK-801 (NMDA receptor antagonist) produced a partial reduction in glutamate-induced activation of the enzyme. MK-801 was not synergistic to L-NAME (NOS inhibitor), suggesting that glutamate stimulates the NMDA-NOS pathway to activate α2,3 Na+K+-ATPase in rat striatum. This regulation was associated with cyclic GMP (but not cyclic AMP) synthesis. These data indicate the existence, in vitro, of a regulatory pathway by which glutamate, acting through NO and cGMP, can cause alterations in striatal α2,3 Na+K+-ATPase activity. Copyright © 2004 John Wiley & Sons, Ltd.
- Publication
Cell Biochemistry & Function, 2005, Vol 23, Issue 2, p115
- ISSN
0263-6484
- Publication type
Article
- DOI
10.1002/cbf.1217