Search

Objective: To study the mechanism of Ca(2+) on the apoptosis induced by hyperthermia in neonate rat hippocampal neurons to provide the applicative evidence of dantrolene for preventing brain injuries., Methods: Dantrolene, Ca(2+) specific blocking agent, was used in the hyperthermia-induced apoptosis of primary hippocampal neurons in vitro to observe its effect on the apoptosis, fluorescent intensity, and dynamic change of Ca(2+) by flowcytometry and laser confocal microscopy., Results: The rate of apoptosis was decreased significantly after hyperthermia treatment by dantrolene sodium. The intracellular Ca(2+) fluorescent intensity in 42 degrees C treatment group (107.35 +/- 6.0) was significantly lower than that in control group (159.12 +/- 33.8). The concentration of Ca(2+) began to decrease 20 approximately 25 s after adding dantrolene sodium, and reached the lowest level about 50 s later, and then kept lower than the basal level., Conclusion: Dantrolene sodium has an important protective effect on hippocampal neurons apoptosis induced by hyperthermia and may have some applicative value of preventing heat-induced brain injury.

Objective: To study the changes of Ca2+ concentration mediated by N-methyl-D-aspartate (NMDA) receptor in the neurons in the preoptic area/anterior hypothalamus (PO/AH) of anoxic SD rats by investigating the properties of NMDA receptor., Methods: The effects of NMDA receptor agonist NMDA and antagonist vaproic acid (VPA) on the [Ca2+]i in PO/AH neurons were observed in SD rats with anoxia., Results: Under normal condition, the fluorescencet ratio was 0.95, which increased obviously in response to treatment with NMDA at 40 s and reached the peak value, 2.054, after 25 s with an increment of (109+/-52) %. After the addition of the agonist, the peak value reached 3.783 in 30 s and maintained the high level. The concentration of Ca2+ increased by (286+/-91) % after the treatment with NMDA. While in the anoxia group, the concentration of Ca2+ decreased by (103+/-45)% after the addition of VPA., Conclusions: The increase in the concentration of Ca2+ results predominantly from the opening of NMDA receptor channel which allows Ca2+ influx. VPA may decrease the activity of NMDA receptor to reduce the Ca2+ concentration for the protection of the neurons against anoxia.