Zanotto L, Heinemann U
Neurosci Lett. 1983 Jan 31;35(1):79-84. doi: 10.1016/0304-3940(83)90530-x.
Extracellular Ca2+ and Na+ were simultaneously measured with ion selective electrodes in the CA1 pyramidal cell layer of rat hippocampal slices. Repetitive stimulation of the Schaffer collateral/commissural fiber system led to decreases in [Ca2+] omicron and [Na+] omicron (delta Ca, delta Na) by up to 0.5 mM and 13 mM, respectively. Iontophoretic application of glutamate or aspartate caused dose-dependent delta Ca of more than 1 mM and delta Na of more than 45 mM. Such ionic alterations were smaller in the presence of GABA or of the Ca2+ antagonists Ni2+ and Mg2+. Ca2+ signals were diminished when evoked in low-Na+ bathing medium and Na+ signals were reduced in Ca2+-free solutions. Thus glutamate- and aspartate-dependent decreases in [Na+] omicron and [Ca2+] omicron appear to be caused by 3 different mechanisms: Na+ movement through amino acid-activated ionophores; Ca2+ movement through selective channels, and Ca2+-dependent Na+ movement.
利用离子选择性电极在大鼠海马脑片的CA1锥体细胞层同时测量细胞外Ca2+和Na+。反复刺激海马伞/联合纤维系统会导致[Ca2+]o和[Na+]o分别下降高达0.5 mM和13 mM（ΔCa，ΔNa）。离子导入谷氨酸或天冬氨酸会引起剂量依赖性的ΔCa超过1 mM和ΔNa超过45 mM。在存在GABA或Ca2+拮抗剂Ni2+和Mg2+的情况下，这种离子变化较小。在低Na+浴液中诱发时Ca2+信号减弱，而在无Ca2+溶液中Na+信号降低。因此，谷氨酸和天冬氨酸依赖性的[Na+]o和[Ca2+]o下降似乎是由3种不同机制引起的：Na+通过氨基酸激活的离子载体移动；Ca2+通过选择性通道移动，以及Ca2+依赖性Na+移动。
