title: Inhibition of ATP-induced Ca2+ influx by corticosterone in dorsal root ganglion neurons.
abstract: In addition to the classic genomic effects, it is well known that glucocorticoids also have rapid, nongenomic effects on neurons. In the present study, the effect of corticosterone (CORT) on ATP-induced Ca(2+) mobilization in cultured dorsal root ganglion (DRG) neurons were detected with confocal laser scanning microscopy using fluo-4/AM as a calcium fluorescent indicator that could monitor real-time alterations of intracellular calcium concentration ([Ca(2+)]i). ATP, an algesic agent, caused [Ca(2+)]i increase in DRG neurons by activation of P2X receptor. Pretreatment with CORT (1 nM-1 microM for 5 min) inhibited ATP-induced [Ca(2+)]i increase in DRG neurons. The rapid inhibition of ATP-induced Ca(2+) response by CORT was concentration-dependent, reversible and could be blocked by glucocorticoid receptor antagonist RU38486 (10 microM). Furthermore, the inhibitory effect of CORT was abolished by protein kinase A inhibitor H89 (10 microM), but was not influenced by protein kinase C inhibitor Chelerythrine chloride (10 microM). On the other hand, membrane-impermeable bovine serum albumin-conjugated corticosterone had no effect on ATP-induced [Ca(2+)]i transients. These observations suggest that a nongenomic pathways may be involved in the effect of CORT on ATP-induced [Ca(2+)]i transients in cultured DRG neurons.
authors.affiliation: Department of Neurobiology, College of Medicine, Third Military Medical University, 30 Gaotanyan Street, 400038, Shapingba District, Chongqing, People's Republic of China.
authors.forename: Xiaohong
authors.initials: X
authors.lastname: Liu
authors.forename: Junwei
authors.initials: J
authors.lastname: Zeng
authors.forename: Yandong
authors.initials: Y
authors.lastname: Zhao
authors.forename: Zhi
authors.initials: Z
authors.lastname: Xiao
authors.forename: Chuanqing
authors.initials: C
authors.lastname: Fang
authors.forename: Huaizhen
authors.initials: H
authors.lastname: Ruan
mesh_terms: D000255:Adenosine Triphosphate / Q000031:analogs & derivatives / Q000037:antagonists & inhibitors / Q000494:pharmacology*; D000818:Animals; D002118:Calcium / Q000378:metabolism*; D003345:Corticosterone / Q000494:pharmacology*; D017868:Cyclic AMP-Dependent Protein Kinases / Q000037:antagonists & inhibitors; D005727:Ganglia, Spinal / Q000187:drug effects* / Q000378:metabolism; D007546:Isoquinolines / Q000494:pharmacology; D015735:Mifepristone / Q000494:pharmacology; D009474:Neurons / Q000187:drug effects / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D011965:Receptors, Glucocorticoid / Q000037:antagonists & inhibitors; D012710:Serum Albumin, Bovine / Q000494:pharmacology; D013449:Sulfonamides / Q000494:pharmacology
chemical_list: D007546:Isoquinolines; D011965:Receptors, Glucocorticoid; D013449:Sulfonamides; C439264:bovine serum albumin-corticosterone conjugate; D012710:Serum Albumin, Bovine; D015735:Mifepristone; C045674:2',3'-O-(2,4,6-trinitro-cyclohexadienylidine)adenosine 5'-triphosphate; D000255:Adenosine Triphosphate; D017868:Cyclic AMP-Dependent Protein Kinases; C063509:N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide; D002118:Calcium; D003345:Corticosterone