Chen C, Kano M, Abeliovich A, Chen L, Bao S, Kim J J, Hashimoto K, Thompson R F, Tonegawa S
Howard Hughes Medical Institute, Center for Learning and Memory, Cambridge, Massachusetts, USA.
Cell. 1995 Dec 29;83(7):1233-42. doi: 10.1016/0092-8674(95)90148-5.
It is generally believed that a smooth execution of a compound movement, or motor coordination, requires learning of component movements as well as experience-based refinement of the motor program as a whole. PKC gamma mutant mice display impaired motor coordination but intact eyeblink conditioning, a form of component movement learning. Cerebellar long-term depression, a putative cellular mechanism for component motor learning, is also unimpaired. Thus, PKC gamma mutant mice are defective in refinement of the motor program. In the accompanying paper, we demonstrate that innervation of multiple climbing fibers onto Purkinje cells persists in adulthood in these mutant mice. We propose that this defective elimination of surplus climbing fibers underlies motor discoordination.
人们普遍认为，复合运动的顺利执行，即运动协调，需要学习组成运动以及基于经验对整个运动程序进行优化。蛋白激酶Cγ（PKCγ）突变小鼠表现出运动协调受损，但眨眼条件反射正常，眨眼条件反射是一种组成运动学习形式。小脑长时程抑制是组成运动学习的一种假定细胞机制，在这些小鼠中也未受损。因此，PKCγ突变小鼠在运动程序优化方面存在缺陷。在随附的论文中，我们证明在这些突变小鼠成年后，多个攀缘纤维对浦肯野细胞的神经支配仍然存在。我们提出，这种多余攀缘纤维的缺陷性消除是运动失调的基础。
