Miyata M, Finch E A, Khiroug L, Hashimoto K, Hayasaka S, Oda S I, Inouye M, Takagishi Y, Augustine G J, Kano M
Laboratory for Cellular Neurophysiology, Brain Science Institute, RIKEN, Saitama, Japan.
Neuron. 2000 Oct;28(1):233-44. doi: 10.1016/s0896-6273(00)00099-4.
We have used rats and mice with mutations in myosin-Va to evaluate the range and function of IP3-mediated Ca2+ signaling in dendritic spines. In these mutants, the endoplasmic reticulum and its attendant IP3 receptors do not enter the postsynaptic spines of parallel fiber synapses on cerebellar Purkinje cells. Long-term synaptic depression (LTD) is absent at the parallel fiber synapses of the mutants, even though the structure and function of these synapses otherwise appear normal. This loss of LTD is associated with selective changes in IP3-mediated Ca2+ signaling in spines and can be rescued by photolysis of a caged Ca2+ compound. Our results reveal that IP3 must release Ca2+ locally in the dendritic spines to produce LTD and indicate that one function of dendritic spines is to target IP3-mediated Ca2+ release to the proper subcellular domain.
我们利用肌球蛋白-Va发生突变的大鼠和小鼠，来评估IP3介导的Ca2+信号在树突棘中的范围和功能。在这些突变体中，内质网及其相关的IP3受体不会进入小脑浦肯野细胞上平行纤维突触的突触后棘。即使这些突触的结构和功能在其他方面看起来正常，突变体的平行纤维突触处也不存在长期突触抑制（LTD）。LTD的这种缺失与棘中IP3介导的Ca2+信号的选择性变化有关，并且可以通过光解笼化Ca2+化合物来挽救。我们的结果表明，IP3必须在树突棘中局部释放Ca2+以产生LTD，并表明树突棘的一个功能是将IP3介导的Ca2+释放靶向到适当的亚细胞结构域。
