Magnoni M S, Govoni S, Battaini F, Trabucchi M
Institute of Pharmacological Sciences, University of Milan, Italy.
J Cereb Blood Flow Metab. 1988 Feb;8(1):96-9. doi: 10.1038/jcbfm.1988.12.
Increasing evidence suggests a role for calcium ions in the pathophysiology of ischemic brain damage. The major mechanism allowing calcium entry from the extracellular compartment is the opening of voltage-operated calcium channels. In this line, we have explored the hypothesis that the characteristics of central L-type voltage-dependent calcium channels, labeled by the dihydropyridine ligand 3H-PN 200-110, may be modified by experimental ischemia. The results show that short-term mild ischemia, produced in the rat by 1 h of right carotid ligation, induces an increase in the number of 3H-PN 200-110 binding sites in the hippocampus ipsilateral to the side of carotid occlusion, accompanied by an increase in the dissociation constant value, whereas no changes in the kinetic parameters of the binding were observed in the other areas examined, i.e., the cortex and the striatum. The changes in hippocampus are transient: 96 h after the occlusion, binding parameters return to the control range. The modifications of the binding characteristics in the hippocampus may be related to alterations of Ca2+ fluxes through L-type calcium channels.
越来越多的证据表明钙离子在缺血性脑损伤的病理生理学中发挥作用。允许钙离子从细胞外间隙进入的主要机制是电压门控钙通道的开放。据此，我们探讨了这样一种假说，即由二氢吡啶配体3H-PN 200-110标记的中枢L型电压依赖性钙通道的特性可能会因实验性缺血而改变。结果表明，通过右侧颈动脉结扎1小时在大鼠中产生的短期轻度缺血，会导致颈动脉闭塞侧同侧海马中3H-PN 200-110结合位点数量增加，同时解离常数增大，而在其他检测区域，即皮层和纹状体中，未观察到结合动力学参数的变化。海马中的这些变化是短暂的：闭塞96小时后，结合参数恢复到对照范围。海马中结合特性的改变可能与通过L型钙通道的Ca2+通量变化有关。
