Medina J I, Barden S D, Davies M S, Newell B A, Shaw S A, Willis M, Halliwell J V
Department of Physiology, Royal Free Hospital School of Medicine, University of London, UK.
Neurosci Lett. 1994 Feb 28;168(1-2):106-10. doi: 10.1016/0304-3940(94)90427-8.
Synaptic transmission in the CA1 area of the hippocampal slice preparation in vitro was studied in bathing media containing different levels of divalent cations. Transmission was abolished by replacing the normal levels (2.5 mM) of Ca2+ with 3 mM Mg. Transmission was not permanently restored by subsequent addition of Ba2+ but added Ca2+ was effective. Transient reappearance of synaptic currents were seen when Ba2+ was added at a time when contaminating levels of Ca2+ were still present, but neurotransmission waned as [Ca2+]e declined with protracted washout. In accordance with this interpretation, Ba2+ potentiated the transmission observed in the presence of low concentrations (0.25 mM) of Ca2+. Little evidence was found for Ba2+ effects at axonal sites but the potentiation of synaptic transmission by Ba2+ could be accounted for in terms of a blockade of terminal K-channels.
在含有不同水平二价阳离子的体外海马脑片制备的CA1区研究了突触传递。用3 mM Mg取代正常水平（2.5 mM）的Ca2+可消除传递。随后添加Ba2+不能使传递永久恢复，但添加Ca2+是有效的。当在仍存在污染水平的Ca2+时添加Ba2+时，可见突触电流短暂重现，但随着[Ca2+]e随着长时间冲洗而下降，神经传递减弱。根据这一解释，Ba2+增强了在低浓度（0.25 mM）Ca2+存在下观察到的传递。几乎没有发现Ba2+对轴突部位有影响的证据，但Ba2+对突触传递的增强作用可以用终末钾通道的阻断来解释。
