RESUMEN
The in vivo action of estradiol was shown to cause changes both in the total amount of phosphoinsitides and their individual fractions of rat synaptosomes. The maximum elevated levels of phosphoinositides was revealed on 1-hour exposure to the hormone. It is suggested the redistribution of phosphoinositides at the primary stage (1 hour postinjection) of exposure may rely on the initiation and functioning of the phosphoinositide mechanism, the ratio of triphosphoinositide to monophosphoinositide may be a peculiar indicator of the status of synaptosomal membranes for the functioning of this regulatory system.
Asunto(s)
Encéfalo/efectos de los fármacos , Estradiol/farmacología , Fosfatidilinositoles/metabolismo , Sinaptosomas/efectos de los fármacos , Animales , Encéfalo/metabolismo , Cromatografía en Capa Delgada , Femenino , Embarazo , Ratas , Sinaptosomas/metabolismoRESUMEN
Spermine decreased distinctly the activity of Ca2+ -phospholipid-dependent protein kinases, whereas not affected the protein kinase A activity. Content of cytosol estradiol receptors was drastically decreased in rat uterine in presence of the polyamine. The data obtained and literature data suggest that activation of estradiol receptors appears to occur after phosphorylation by means of Ca2+ - dependent protein kinases, which are regulated via phosphoinositide-involving mechanism, i.e. these receptors acquire the ability to bind hormones.