Role of IP_3 receptor/Ca^<2+> signaling in neural plasticity and brain development

我们发现，波和Ca ~（2+）振荡是通过位于内质网的Ca ~（2+）通道产生的，而不是通过质膜上的Ca ~（2+）通道产生的，因此我们采用激光辅助的卡利（chromophore assisted laser inactivation）方法研究了IP_3受体介导的Ca ~（2+）运动是否参与了生长锥的形成和突起的延伸。我们用孔雀石绿绿色标记抗1型IP 3受体的特异性抗体。我们将激光束加入染料中以产生标记物，对照抗体显示不阻断神经突的延伸，而抗IP 3型抗体显示只有在生长锥处加入激光时才能引起神经突的收缩，这表明IP 3受体介导的Ca ~（2+）释放参与了神经突的延伸。

We have found that wave and Ca2+ oscillation is produced through the Ca2+ channel localized on the endoplasmic reticulum which is a Ca2+ store site inside the cell, and not through Ca2+ channel on the plasma membrane.We used CALI(chromophore assisted laser inactivation)method using laser beam to study if IP3 receptor mediated Ca2+ movement is involved in growth cone formation and neurite extention. We used malakite green to label specific antibody against type 1 IP3 receptor. We added laser beam to the dye to produce redicals.While control antibody showed no block in neurite extention, antibody against type IP3 showed retraction of neurite, only when laser is added at growth cone.This suggests that IP3 receptor medited Ca2+ release is involved in neurite extention.