Elife. 2019 Sep 05. pii: e45590. [Epub ahead of print]8
Bin Wu,
François G C Blot,
Aaron Benson Wong,
Catarina Osório,
Youri Adolfs,
R Jeroen Pasterkamp,
Jana Hartmann,
Esther B E Becker,
Henk-Jan Boele,
Chris I De Zeeuw,
Martijn Schonewille.
Despite the canonical homogeneous character of its organization, the cerebellum plays differential computational roles in distinct sensorimotor behaviors. Previously we showed that Purkinje cell activity differs between zebrin-negative (Z-) and zebrin-positive (Z+) modules (Zhou et al., 2014). Here, using gain-of-function and loss-of-function mouse models, we show that transient receptor potential cation channel C3 (TRPC3) controls the simple spike activity of Z-, but not Z+ Purkinje cells. In addition, TRPC3 regulates complex spike rate and their interaction with simple spikes, exclusively in Z- Purkinje cells. At the behavioral level, TRPC3 loss-of-function mice show impaired eyeblink conditioning, which is related to Z- modules, whereas compensatory eye movement adaptation, linked to Z+ modules, is intact. Together, our results indicate that TRPC3 is a major contributor to the cellular heterogeneity that introduces distinct physiological properties in Purkinje cells, conjuring functional heterogeneity in cerebellar sensorimotor integration.
Keywords: mouse; neuroscience