Aim:In our previous observations,adenosine triphosphate(ATP)was found toevoke immediate elevations in intracellular free calcium concentration([Ca~(2+)]_i)in HT4 neuroblastoma cells of mice.We tried to see if a brief pretreatment ofglucocorticoids could inhibit the Ca~(2+)response and reveal the underlying signal-ing mechanism.Methods:Measurement of[Ca~(2+)]_i was carried out using thedual-wavelength fluorescence method with Fura-2 as the indicator.Results:Pre-incubation of HT4 cells for 5 min with corticosterone(B)or bovine serum albu-min conjugated corticosterone(B-BSA)inhibited the peak[Ca~(2+)]_i increments in aconcentration-dependent manner.Cortisol and dexamethasone had a similar action,while deoxycorticosterone and cholesterol were ineffective.Both extracellularCa~(2+)influx and intemal Ca~(2+)release contributed to ATP-induced[Ca~(2+)]_i elevation.The brief treatment with only B attenuated Ca~(2+)influx.Furthermore,the[Ca~(2+)]_ielevation induced by the P2X receptor agonist adenosine 5’-(β,γ-methylene)triph-osphate(β,γ-meATP)was also suppressed.The rapid inhibitory effect of B canbe reproduced by forskolin 1 mmol/L and blocked by H89 20 mmol/L.Neithernuclear glucocorticoid receptor antagonist mifepristone nor protein kinase C in-hibitors influenced the rapid action of B.Conclusion:Our results suggest thatglucocorticoids modulate P2X receptor-medicated Ca~(2+)influx through a mem-brane-initiated,non-genomic and PKA-dependent pathway in HT4 cells. Aim: In our previous observations, adenosine triphosphate (ATP) was found to evoke immediate elevations in intracellular free calcium concentration ([Ca ~ (2 +)] _i) in HT4 neuroblastoma cells of mice. We tried to see if a brief pretreatment of glucocorticoids could inhibit the Ca 2+ response and reveal the underlying signal-ing mechanism. Methods: Measurement of [Ca ~ (2 +)] _i was carried out using thedual-wavelength fluorescence method with Fura-2 as the indicator. Results: Pre-incubation of HT4 cells for 5 min with corticosterone (B) or bovine serum albu-min conjugated corticosterone (B-BSA) inhibited the peak [Ca ~ (2 +)] _ i increments in aconcentration-dependent manner. Cortisol and dexamethasone had a similar action, while deoxycorticosterone and cholesterol were ineffective.Both extracellular Ca ~ (2+) influx and intemal Ca ~ (2+) release contributed to ATP-induced [Ca ~ (2 +)] _i elevation.The brief treatment with only B attenuated Ca ~ (2+) influx.Furthermore, the [Ca ~ (2 +)] _levenvation induced by the P2X receptor agonist address NOSINE 5 ’- (β, γ-methylene) triph-osphate (β, γ-meATP) was also suppressed. The rapid inhibitory effect of B canbe reproduced by forskolin 1 mmol / L and blocked by H89 20 mmol / L.Neithernuclear glucocorticoid receptor antagonist mifepristone nor protein kinase C in-hibitors influenced the rapid action of B. Conlusion: Our results suggest that glucocorticoids modulate P2X receptor-medicated Ca 2+ influx through a mem-brane-initiated, non-genomic and PKA-dependent pathway in HT4 cells.