降钙素基因相关肽对培养的大鼠神经元中电压激活通道的调节作用。
Modulation of voltage-activated channels by calcitonin gene-related peptide in cultured rat neurones.
作者信息
Zona C, Farini D, Palma E, Eusebi F
机构信息
Dipartimento di Medicina Sperimentale, Universitá dell'Aquila, Italy.
出版信息
J Physiol. 1991 Feb;433:631-43. doi: 10.1113/jphysiol.1991.sp018447.
Abstract
- Whole-cell currents were recorded from cultures of dissociated neocortical neurones of the rat. Rat alpha-calcitonin gene-related peptide (CGRP; 1 nM-1 microM) caused significant dose-dependent decreases in the voltage-activated transient (A-current) and delayed rectifier K+ currents. Forskolin (10 nM-20 microM) mimicked this effect. Peak K+ currents were gradually decreased after loading neurones with cyclic AMP (100 microM) through patch pipettes. CGRP was ineffective in neurones loaded with cyclic AMP. 2. CGRP (0.5-2 microM) increased cytosolic cyclic AMP concentration and this effect was mimicked by forskolin (5-40 microM). 3. CGRP (0.1-1 microM) reduced high-threshold Ca2+ currents; as did forskolin (5-20 microM) and cyclic AMP loaded into the neurones. In contrast, low-threshold Ca2+ currents were not affected by any of these agents. 4. Voltage-activated Na+ currents were significantly reduced by both CGRP (0.1-1 microM) and forskolin (5-20 microM). A similar effect was observed when cells were loaded with cyclic AMP. 5. We conclude that, in neocortical neurones, CGRP attenuates voltage-activated currents by stimulating the intracellular cyclic AMP signalling system.
摘要
- 从大鼠分离的新皮质神经元培养物中记录全细胞电流。大鼠α-降钙素基因相关肽（CGRP；1 nM - 1 μM）导致电压激活的瞬时（A电流）和延迟整流钾电流出现显著的剂量依赖性降低。福斯高林（10 nM - 20 μM）模拟了这种效应。通过膜片吸管向神经元加载环磷酸腺苷（100 μM）后，钾电流峰值逐渐降低。CGRP对加载了环磷酸腺苷的神经元无效。2. CGRP（0.5 - 2 μM）增加了细胞溶质环磷酸腺苷浓度，福斯高林（5 - 40 μM）模拟了这种效应。3. CGRP（0.1 - 1 μM）降低了高阈值钙电流；福斯高林（5 - 20 μM）和加载到神经元中的环磷酸腺苷也有同样效果。相比之下，低阈值钙电流不受这些药物中任何一种影响。4. CGRP（0.1 - 1 μM）和福斯高林（5 - 20 μM）均显著降低了电压激活的钠电流。当细胞加载环磷酸腺苷时也观察到类似效应。5. 我们得出结论，在新皮质神经元中，CGRP通过刺激细胞内环磷酸腺苷信号系统减弱电压激活电流。
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