Effects of dexamethasone on intracellular Ca2+ in its sensitive cells from neonatal mouse hippocampus and cultured cortical neurogliocytes
Abstract
AIM:
To investigate the effects of dexamethasone (Dex) on intracellular free calcium ([Ca2+]i) in the single neuron or neurogliocyte.
METHODS:
Neonatal mouse hippocampal cells (NMHC) and cultured cortical neurogliocytes (CCN) were loaded with Fura 2-AM. The [Ca2+]i was measured with AR-CM-MIC-cation measurement system.
RESULTS:
Most of freshly isolated NMHC exhibited a rapid and concentration-dependent [Ca2+]i increase after administration of Dex 40-200 mumol.L-1. Only 10% of NMHC showed their [Ca2+]i decreases in total 96 tested cells. Dex-triggered [Ca2+]i rise was prevented by incubating the cells with Mg(2+)-free solution and reduced by adding LaCl3. Suspended NMHC in Ca(2+)-free solution or pretreated cells with mifepristone or tetrodotoxin prevented the initial [Ca2+]i increases caused by Dex 40-90 mumol.L-1, but only diminished the later [Ca2+]i rises by Dex 200 mumol.L-1. About 50% of tested single CCN showed a rapid and concentration-related [Ca2+]i increase due to Dex 90-270 mumol.L-1 exposure. This effect was partially inhibited under extracellular Ca(2+)- or Mg(2+)-free and mifepristone pretreatment conditions.
CONCLUSION:
Dex produces the rapid [Ca2+]i changes in both neurons and glia cells. Reactions among most cells include a Mg(2+)-dependent and glucocorticoid receptor-related extracellular Ca2+ influx and a high concentration of Dex-mediated intracellular Ca2+ release.
Keywords:
To investigate the effects of dexamethasone (Dex) on intracellular free calcium ([Ca2+]i) in the single neuron or neurogliocyte.
METHODS:
Neonatal mouse hippocampal cells (NMHC) and cultured cortical neurogliocytes (CCN) were loaded with Fura 2-AM. The [Ca2+]i was measured with AR-CM-MIC-cation measurement system.
RESULTS:
Most of freshly isolated NMHC exhibited a rapid and concentration-dependent [Ca2+]i increase after administration of Dex 40-200 mumol.L-1. Only 10% of NMHC showed their [Ca2+]i decreases in total 96 tested cells. Dex-triggered [Ca2+]i rise was prevented by incubating the cells with Mg(2+)-free solution and reduced by adding LaCl3. Suspended NMHC in Ca(2+)-free solution or pretreated cells with mifepristone or tetrodotoxin prevented the initial [Ca2+]i increases caused by Dex 40-90 mumol.L-1, but only diminished the later [Ca2+]i rises by Dex 200 mumol.L-1. About 50% of tested single CCN showed a rapid and concentration-related [Ca2+]i increase due to Dex 90-270 mumol.L-1 exposure. This effect was partially inhibited under extracellular Ca(2+)- or Mg(2+)-free and mifepristone pretreatment conditions.
CONCLUSION:
Dex produces the rapid [Ca2+]i changes in both neurons and glia cells. Reactions among most cells include a Mg(2+)-dependent and glucocorticoid receptor-related extracellular Ca2+ influx and a high concentration of Dex-mediated intracellular Ca2+ release.