Abstract:
:There is growing evidence on the existence of endogenous ouabain-like factors that modulate Na+, K(+)-ATPase activity. In this laboratory, two soluble subfractions (peaks I and II) were previously separated from rat cerebral cortex, which had opposite effects on Na+, K(+)-ATPase activity. Peak I stimulated and peak II inhibited the enzyme (Rodríguez de Lores Arnaiz and Antonelli de Gómez de Lima, Neurochem Res 11:933-947, 1986). The same effects are now reported for K(+)-p-nitrophenyphosphatase activity. Localization of high-affinity ouabain binding in rat brain was done by quantitative autoradiography using a microcomputer digital imaging system. Peak I did not modify, whereas peak II blocked ouabain binding in areas 3-4 of cerebral cortex, dentate gyrus, stria terminalis, thalamic nuclei, and basal ganglia. Similar results were obtained when ouabain binding was determined in rabbit cerebral cortex and by a conventional filtration assay in nerve ending membranes obtained from rat cerebral cortex. These results favour the idea that the factor present in peak II fraction might behave as an ouabain-like substance.
journal_name
J Neurosci Resjournal_title
Journal of neuroscience researchauthors
Antonelli M,Casillas T,Rodríguez de Lores Arnaiz Gdoi
10.1002/jnr.490280303keywords:
subject
Has Abstractpub_date
1991-03-01 00:00:00pages
324-31issue
3eissn
0360-4012issn
1097-4547journal_volume
28pub_type
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