Eriksson P S, Nilsson M, Wågberg M, Hansson E, Rönnbäck L
Institute of Neurobiology, University of Göteborg, Sweden.
Neuroscience. 1993 May;54(2):401-7. doi: 10.1016/0306-4522(93)90261-d.
Cultured astrocytes from the cerebral cortex of the rat respond to opioid kappa-receptor stimulation with a substantial elevation of the cytoplasmic free calcium, visualized through the use of the fluorescent calcium indicator Fura-2. The stimulation of kappa-receptors with U-50488H increases the level of calcium through a dose-related stimulatory effect on the transmembrane calcium influx. The kappa-receptor stimulation was completely blocked by the selective kappa-receptor blocker nor-binaltorphimine. Furthermore, the transmembrane calcium influx was completely blocked by nifedipine, indicating the involvement of L-type channels. The presence of L-type channels was verified by stimulation of L-type channels with Bay K8644. The effects of Bay K8644 were completely blocked by nifedipine. L-type channel-coupled kappa-receptors on astrocytes might represent a novel mechanism contributing to the depressant action of opioids on synaptic transmission via decreasing the availability of extracellular calcium necessary for presynaptic transmitter release.
通过使用荧光钙指示剂Fura-2可视化发现，从大鼠大脑皮质培养的星形胶质细胞对阿片κ受体刺激有反应，细胞质游离钙大幅升高。用U-50488H刺激κ受体通过对跨膜钙内流的剂量相关刺激作用来增加钙水平。选择性κ受体阻滞剂诺-纳曲酮完全阻断了κ受体刺激。此外，硝苯地平完全阻断了跨膜钙内流，表明L型通道参与其中。用Bay K8644刺激L型通道证实了L型通道的存在。硝苯地平完全阻断了Bay K8644的作用。星形胶质细胞上L型通道偶联的κ受体可能代表一种新机制，通过降低突触前递质释放所需的细胞外钙的可用性，导致阿片类药物对突触传递的抑制作用。
