Deletion of the ryanodine receptor type 3 (RyR3) impairs forms of synaptic plasticity and spatial learning
Deletion of the ryanodine receptor type 3 (RyR3) impairs forms of synaptic plasticity and spatial learning
复制标题
DOI：
10.1093/emboj/18.19.5264
复制
发表时间：
1999-10-01
期刊：
影响因子：
11.4
通讯作者：
Sorrentino, V
中科院分区：
文献类型：
--
作者：
Balschun, D;Wolfer, DP;Sorrentino, V
删除 3 型兰尼碱受体 (RyR3) 会导致海马突触可塑性发生特定变化，但不会影响海马形态、基础突触传递或突触前功能。在体外海马切片中，由 CA1 区和齿状回重复、强烈强直作用诱导的鲁棒长时程增强 (LTP) 没有改变，而由单次弱强直作用或强弱 LTP 去弱化产生的弱形式可塑性受到损害。这些明显的生理缺陷与在水迷宫中重新学习新目标的灵活性的降低相平行。相比之下，突变体和野生型同窝小鼠在获取阶段和探索试验期间的学习表现没有差异。在旷场中，RyR3(-/-)小鼠表现出正常的探索和习惯，但运动速度加快，并有轻微的圆周跑倾向。观察到的生理和行为效应表明 RyR3 介导的 Ca2+ 释放参与了空间学习和海马突触可塑性的细胞内过程。
Deletion of the ryanodine receptor type 3 (RyR3) results in specific changes in hippocampal synaptic plasticity, without affecting hippocampal morphology, basal synaptic transmission or presynaptic function. Robust long-term potentiation (LTP) induced by repeated, strong tetanization in the CA1 region and in the dentate gyrus was unaltered in hippocampal slices iii vitro, whereas weak forms of plasticity generated by either a single weak tetanization or depotentiation of a robust LTP were impaired. These distinct physiological deficits were paralleled by a reduced flexibility in relearning a new target in the water-maze. In contrast, learning performance in the acquisition phase and during probe trial did not differ between the mutants and their wild-type littermates. In the open-field, RyR3(-/-) mice displayed a normal exploration and habituation, but had an increased speed of locomotion and a mild tendency to circular running. The observed physiological and behavioral effects implicate RyR3-mediated Ca2+ release in the intracellular processes underlying spatial learning and hippocampal synaptic plasticity.