Inhibition gates supralinear Ca2+ signaling in purkinje cell dendrites during practiced movements

• Type of Material: Article
• Authors: Michael A. Gaffield, Max Planck Florida Institute for Neuroscience; Matt Rowan, Emory University; Samantha B. Amat, Max Planck Florida Institute for Neuroscience; Hirokazu Hirai, Graduate School of Medicine; Jason M. Christie, Max Planck Florida Institute for Neuroscience
• Language: English
• Date: 2018-08-17
• Publisher: eLife
• Publication Version: Final Published Version
• Copyright Statement: © 2018, Gaffield et al
• License: Creative Commons Attribution 4.0 International
• Final Published Version (URL): http://dx.doi.org/10.7554/eLife.36246
• Title of Journal or Parent Work: eLife
• Volume: 7
• Grant/Funding Information: This work was supported by the Max Planck Society, the Max Planck Florida Institute for Neuroscience, and National Institutes of Health Grant NS083894 (JMC).
• Keywords: Synapses; Animals; cerebellum; Purkinje Cells; neuroscience; mouse; Interneurons; Cerebellar Cortex; Learning; Evoked Potentials, Motor; Calcium Signaling; Dendrites; Movement; Patch-Clamp Techniques; inhibition; Excitatory Postsynaptic Potentials; Mice; calcium
• Research Categories: Biology, Neuroscience

Abstract

Motor learning involves neural circuit modifications in the cerebellar cortex, likely through re-weighting of parallel fiber inputs onto Purkinje cells (PCs). Climbing fibers instruct these synaptic modifications when they excite PCs in conjunction with parallel fiber activity, a pairing that enhances climbing fiber-evoked Ca2+ signaling in PC dendrites. In vivo, climbing fibers spike continuously, including during movements when parallel fibers are simultaneously conveying sensorimotor information to PCs. Whether parallel fiber activity enhances climbing fiber Ca2+ signaling during motor behaviors is unknown. In mice, we found that inhibitory molecular layer interneurons (MLIs), activated by parallel fibers during practiced movements, suppressed parallel fiber enhancement of climbing fiber Ca2+ signaling in PCs. Similar results were obtained in acute slices for brief parallel fiber stimuli. Interestingly, more prolonged parallel fiber excitation revealed latent supralinear Ca2+ signaling. Therefore, the balance of parallel fiber and MLI input onto PCs regulates concomitant climbing fiber Ca2+ signaling.