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Dramatic effects of external alkalinity on neuronal calcium recovery following a short‐duration glutamate challenge: the role of the plasma membrane Ca 2+ /H + pump
Author(s) -
Khodorov Bi,
V. G. Pinelis,
O Vergun,
T. P. Storozhevykh,
D. Fajuk,
N. Vinskaya,
E. Arsenjeva,
Л. Г. Хаспеков,
A. Lyzin,
N. K. Isaev,
N. A. Andreeva,
Ilya V. Victorov
Publication year - 1995
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(95)00894-f
Subject(s) - chemistry , glutamate receptor , calcium , biophysics , nmda receptor , hippocampal formation , granule (geology) , biochemistry , endocrinology , biology , paleontology , receptor , organic chemistry
Alkalinization of the external medium has been shown to suppress Ca 2+ extrusion from neurons due to inhibition of the plasmalemmal Ca 2+ /H + pump. In our experiments on fura‐2‐loaded rat cerebellar granule cells and mouse hippocampal neurons, an increase in pH o from 7.4 to 8.5 following a 1‐min glutamate or NMDA challenge caused a dramatic delay in [Ca 2+ ] i recovery which in some cases was accompanied by an additional increase in [Ca 2+ ] i . Normalization of pH o , or removal of Ca 2+ from the alkaline solution allowed [Ca 2+ ] i to decrease rapidly again. External alkalinity did not affect the initial rapid decline in [Ca 2+ ] i following a 25 mM K + pulse. In cerebellar granule cells, the alkaline pH o considerably increased the 45 Ca 2+ uptake both at rest and following a 2‐min GLU pulse. A comparison of these effects of alkaline pH o with those produced by removal of the external Na + led us to conclude that the Ca 2+ /H + pump plays a dominant role in the mechanism of the fast Ca 2+ extrusion from glutamate‐ or NMDA‐treated neurons.