期刊名称：Proceedings of the National Academy of Sciences
印刷版ISSN：0027-8424
电子版ISSN：1091-6490
出版年度：1998
卷号：95
期号：26
页码：15724-15729
DOI：10.1073/pnas.95.26.15724
语种：English
出版社：The National Academy of Sciences of the United States of America
摘要：Elimination of excess climbing fiber (CF)-Purkinje cell synapses during cerebellar development involves a signaling pathway that includes type 1 metabotropic glutamate receptor, Gq, and the {gamma} isoform of protein kinase C. To identify phospholipase C (PLC) isoforms involved in this process, we generated mice deficient in PLC{beta}4, one of two major isoforms expressed in Purkinje cells. PLC{beta}4 mutant mice are viable but exhibit locomotor ataxia. Their cerebellar histology, parallel fiber synapse formation, and basic electrophysiology appear normal. However, developmental elimination of multiple CF innervation clearly is impaired in the rostral portion of the cerebellar vermis, in which PLC{beta}4 mRNA is predominantly expressed. By contrast, CF synapse elimination is normal in the caudal cerebellum, in which low levels of PLC{beta}4 mRNA but reciprocally high levels of PLC{beta}3 mRNA are found. These results indicate that PLC{beta}4 transduces signals that are required for CF synapse elimination in the rostral cerebellum.
