Estradiol receptors mediate estradiol-induced inhibition of mitochondrial Ca2+ efflux in rat caudate nucleus and brain stem
2015
Аутори:
Petrovic, SnjezanaMilosevic, Maja
Ristic-Medic, Danijela
Velickovic, Natasa
Drakulic, Dunja
Grkovic, Ivana
Horvat, Anica
Тип документа:
Чланак у часопису (Објављена верзија)
Метаподаци
Приказ свих података о документуАпстракт:
Our earlier studies found that in vitro estradiol modulates
mitochondrial Ca2+ transport in discrete brain regions. The present
study examined the role of estradiol receptors (ERs) in
estradiol-induced inhibition of Ca2+ efflux from synaptosomal
mitochondria isolated from rat caudate nuclei and brain stems.
Radioactively labeled CaCl2 (0.6-0.75 mu Ci (CaCl2)-Ca-45) was used for
Ca2+ transport monitoring. The results revealed that in the presence of
ER antagonist 7 alpha, 17 beta-{[}9{[}(4,4,5,5,5-pentafluoropentyl)
sulfinyl] nonyl] estra-1,3,5( 10)-triene-3,17-diol (ICI 182,780) (1 mu
mol/L), the inhibitory effect of estradiol on mitochondrial Ca2+ efflux
was more than 60\% decreased, suggesting the involvement of ER in this
mode of estradiol neuromodulatory action. When particular contributions
of ER alpha and ER beta were tested, it was found that ER beta agonist
2,3-bis(4-hydroxy phenyl)-propionitrile (10 nmol/L) inhibited Ca2+
efflux more than 20\%, while the inhibition with ER alpha agonist 4,4',
4''-(4-propyl-{[}1H]-pyrazole-1,3,5-triyl) trisphenol (10 nmol/L) was
about 10\%, both compared to the control. Both agonists demonstrated
attenuation of Ca2+ efflux decrease in the presence of mitochondrial
Na+/Ca2+ exchanger antagonist
7-chloro-5-(2-chlorophenyl)-1,5-dihyhdro-4,1-benzothiazepin-2(3H)-one
(10 mu mol/L), showing interference with the inhibitory action of that
agent. Our results strongly indicate ERs as the mediators of
estradiol-induced mitochondrial Ca2+ efflux inhibition in rat caudate
nucleus and brain stem synaptosomes.
Кључне речи:
Ca2+ efflux; estradiol receptors; synaptosomal mitochondria; caudate nucleus; brain stemИзвор:
Turkish Journal of Biology, 2015, 39, 2, 328-334
DOI: 10.3906/biy-1408-62
ISSN: 1303-6092