Neary J T, Woodson C, Blicharska J, Norenberg L O, Norenberg M D
Laboratory of Neuropathology, Veterans Administration Medical Center, Miami, FL 33125.
Brain Res. 1990 Aug 6;524(2):231-5. doi: 10.1016/0006-8993(90)90696-9.
Calcium influx, accumulation and efflux were studied in primary cultures of rat astrocytes treated with ammonium chloride. Treatment of the cells for 3 days with 10 mMN4Cl resulted in a 35% reduction in 45Ca influx. The decrease in calcium influx was dose-dependent between 2 and 10 mM NH4Cl. Short-term (30 min) exposure to ammonia had no effect on calcium influx. Calcium accumulation, as measured by 20-min exposure to 45Ca, decreased after treating cultures with 10 mM NH4Cl for one or 3 days; a greater effect was observed after the 3-day treatment. Studies with lanthanum, an inhibitor of calcium transport, indicated that the effect of ammonia was not due to non-specific leakage of calcium. Calcium efflux was not affected by exposure of the cultures to ammonium chloride. Purinergic-evoked calcium influx and mobilization was not altered by ammonia. While the mechanism(s) of calcium homeostasis affected by long-term hyperammonemia remain to be defined, these results suggest that reduced astrocytic calcium may be related to the pathogenesis of ammonia-related disorders such as hepatic encephalopathy.
在氯化铵处理的大鼠星形胶质细胞原代培养物中研究了钙内流、积累和外流。用10 mM氯化铵处理细胞3天导致45Ca内流减少35%。在2至10 mM氯化铵之间，钙内流的减少呈剂量依赖性。短期（30分钟）暴露于氨对钙内流没有影响。在用10 mM氯化铵处理培养物1天或3天后，通过暴露于45Ca 20分钟测量的钙积累减少；在3天处理后观察到更大的影响。用钙转运抑制剂镧进行的研究表明，氨的作用不是由于钙的非特异性泄漏。氯化铵暴露对培养物的钙外流没有影响。氨不会改变嘌呤能诱发的钙内流和动员。虽然长期高氨血症影响钙稳态的机制仍有待确定，但这些结果表明星形胶质细胞钙减少可能与肝性脑病等氨相关疾病的发病机制有关。
