Pivovarov A S, Kotliar B I
Zh Vyssh Nerv Deiat Im I P Pavlova. 1990 Jan-Feb;40(1):135-42.
Pharmacological influences, changing intracellular content of Ca2+, reversibly change the speed and depth of extinction of the input current of the Helix RPa3 and LPa3 neurones, elicited by a repeated iontophoretic application of acetylcholine to the soma. Suppression by extracellular medium, devoid of Ca2+ and by verapamyl (100-150 mumol/l) of Ca2+ input to the cell, induced by cholinoreceptors activation, reversibly weakens the extinction. Raise of intracellular Ca2+ level by blockade with ruthenium red (5-10 mumol/l) of specific Ca2+ transport by mitochondria and by mobilization with caffeine (1-4 mmol/l) of Ca2+, deposited by endoplasmic reticulum, accelerates and intensifies the extinction. The obtained results testify that the short-term cholinoreceptors plasticity of the above neurones is positively controlled by Ca2+ entering the cell by chemically controlled ion channels and mobilized from intracellular Ca-depot.
药理学影响通过改变细胞内Ca2+含量，可逆地改变了将乙酰胆碱反复离子导入螺旋神经节RPa3和LPa3神经元胞体所引发的输入电流的消退速度和深度。细胞外无Ca2+的培养基以及维拉帕米（100 - 150 μmol/l）对胆碱受体激活所诱导的细胞Ca2+内流的抑制，可逆地减弱了消退。用钌红（5 - 10 μmol/l）阻断线粒体特异性Ca2+转运以及用咖啡因（1 - 4 mmol/l）动员内质网储存的Ca2+来提高细胞内Ca2+水平，会加速并增强消退。所得结果证明，上述神经元的短期胆碱受体可塑性受到通过化学控制离子通道进入细胞并从细胞内钙库动员的Ca2+的正向调控。
