Department of Physiology, Seoul National University College of Medicine, Seoul, Republic of Korea; Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul, Republic of Korea; Neuroscience Research Institute, Seoul National University College of Medicine, Seoul, Republic of Korea; Department of Physiology, College of Korean Medicine, Kyung Hee University, Seoul, Republic of Korea; Department of Neuroscience, School of Medicine, Johns Hopkins University, Baltimore, United States
Seung Ha Kim
Department of Physiology, Seoul National University College of Medicine, Seoul, Republic of Korea; Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul, Republic of Korea
Department of Physiology, Seoul National University College of Medicine, Seoul, Republic of Korea; Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul, Republic of Korea; Neuroscience Research Institute, Seoul National University College of Medicine, Seoul, Republic of Korea
Chang-Eop Kim
Department of Physiology, Seoul National University College of Medicine, Seoul, Republic of Korea; Department of Physiology, College of Korean Medicine, Gacheon University, Seongnam, Republic of Korea
Yong Gyu Kim
Department of Physiology, Seoul National University College of Medicine, Seoul, Republic of Korea; Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul, Republic of Korea; Neuroscience Research Institute, Seoul National University College of Medicine, Seoul, Republic of Korea
Department of Physiology, Seoul National University College of Medicine, Seoul, Republic of Korea; Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul, Republic of Korea; Neuroscience Research Institute, Seoul National University College of Medicine, Seoul, Republic of Korea
Climbing fibers (CFs) generate complex spikes (CS) and Ca2+ transients in cerebellar Purkinje cells (PCs), serving as instructive signals. The so-called 'all-or-none' character of CSs has been questioned since the CF burst was described. Although recent studies have indicated a sensory-driven enhancement of PC Ca2+ signals, how CF responds to sensory events and contributes to PC dendritic Ca2+ and CS remains unexplored. Here, single or simultaneous Ca2+ imaging of CFs and PCs in awake mice revealed the presynaptic CF Ca2+ amplitude encoded the sensory input’s strength and directly influenced post-synaptic PC dendritic Ca2+ amplitude. The sensory-driven variability in CF Ca2+ amplitude depended on the number of spikes in the CF burst. Finally, the spike number of the CF burst determined the PC Ca2+ influx and CS properties. These results reveal the direct translation of sensory information-coding CF inputs into PC Ca2+, suggesting the sophisticated role of CFs as error signals.
