Khodorov B, Pinelis V, Vergun O, Storozhevykh T, Fajuk D, Vinskaya N, Arsenjeva E, Khaspekov L, Lyzin A, Isaev N
Institute of General Pathology and Pathophysiology, Russian Academy of Medical Sciences, Moscow.
FEBS Lett. 1995 Sep 11;371(3):249-52. doi: 10.1016/0014-5793(95)00894-f.
Alkalinization of the external medium has been shown to suppress Ca2+ extrusion from neurons due to inhibition of the plasmalemmal Ca2+/H+ pump. In our experiments on fura-2-loaded rat cerebellar granule cells and mouse hippocampal neurons, an increase in pHo from 7.4 to 8.5 following a 1-min glutamate or NMDA challenge caused a dramatic delay in [Ca2+]i recovery which in some cases was accompanied by an additional increase in [Ca2+]i. Normalization of pHo, or removal of Ca2+ from the alkaline solution allowed [Ca2+]i to decrease rapidly again. External alkalinity did not affect the initial rapid decline in [Ca2+]i following a 25 mMK+ pulse. In cerebellar granule cells, the alkaline pHo considerably increased the 45Ca2+ uptake both at rest and following a 2-min GLU pulse. A comparison of these effects of alkaline pHo with those produced by removal of the external Na+ led us to conclude that the Ca2+/H+ pump plays a dominant role in the mechanism of the fast Ca2+ extrusion from glutamate- or NMDA-treated neurons.
外部介质的碱化已被证明会抑制神经元中Ca2+的外流，这是由于质膜Ca2+/H+泵受到抑制。在我们对用fura-2标记的大鼠小脑颗粒细胞和小鼠海马神经元进行的实验中，在1分钟的谷氨酸或NMDA刺激后，细胞外pH值（pHo）从7.4升高到8.5，导致[Ca2+]i恢复出现显著延迟，在某些情况下还伴随着[Ca2+]i的进一步升高。将pHo恢复正常，或从碱性溶液中去除Ca2+，可使[Ca2+]i再次迅速下降。外部碱化并不影响25 mM K+脉冲后[Ca2+]i最初的快速下降。在小脑颗粒细胞中，碱性pHo在静息状态和2分钟谷氨酸脉冲后均显著增加了45Ca2+的摄取。将碱性pHo的这些作用与去除外部Na+所产生的作用进行比较，我们得出结论，Ca2+/H+泵在谷氨酸或NMDA处理的神经元快速Ca2+外流机制中起主导作用。
