Barski, JJ;
Hartmann, J;
Rose, CR;
Hoebeek, F;
Morl, K;
Noll-Hussong, M;
De Zeeuw, CI;
... Meyer, M; + view all
(2003)
Calbindin in cerebellar Purkinje cells is a critical determinant of the precision of motor coordination.
Journal of Neuroscience
, 23
(8)
3469 - 3477.
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Abstract
Long-term depression (LTD) of Purkinje cell-parallel fiber synaptic transmission is a critical determinant of normal cerebellar function. Impairment of LTD through, for example, disruption of the metabotropic glutamate receptor-IP3-calcium signaling cascade in mutant mice results in severe deficits of both synaptic transmission and cerebellar motor control. Here, we demonstrate that selective genetic deletion of the calcium-binding protein calbindin D-28k (calbindin) from cerebellar Purkinje cells results in distinctly different cellular and behavioral alterations. These mutants display marked permanent deficits of motor coordination and sensory processing. This occurs in the absence of alterations in a form of LTD implicated in the control of behavior. Analysis of synaptically evoked calcium transients in spines and dendrites of Purkinje cells demonstrated an alteration of time course and amplitude of fast calcium transients after parallel or climbing fiber stimulation. By contrast, the delayed metabotropic glutamate receptor-mediated calcium transients were normal. Our results reveal a unique role of Purkinje cell calbindin in a specific form of motor control and suggest that rapid calcium buffering may directly control behaviorally relevant neuronal signal integration
| Type: | Article |
|---|---|
| Title: | Calbindin in cerebellar Purkinje cells is a critical determinant of the precision of motor coordination |
| Open access status: | An open access version is available from UCL Discovery |
| Language: | English |
| Additional information: | DA - 20030428 IS - 1529-2401 LA - eng PT - Journal Article RN - 0 (Calcium-Binding Protein, Vitamin D-Dependent) RN - 0 (calbindin) SB - IM This work is licensed under the Creative Commons Attribution-NonCommercial-ShareAlike 3.0 Unported License. The license allows you to copy, distribute, and transmit the work, as well as adapting it. However, you must attribute the work to the author (but not in any way that suggests that they endorse you or your use of the work), and cannot use the work for commercial purposes without prior permission of the author. If you alter or build upon this work, you can distribute the resulting work only under the same or similar license to this one. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-sa/3.0/ or send a letter to Creative Commons, 444 Castro Street, Suite 900, Mountain View, California, 94041, USA. |
| Keywords: | ABSENCE, action potentials, amplitude, analysis, Animals, BEHAVIOR, calcium, Calcium Signaling, Calcium-Binding Protein, Vitamin D-Dependent, CASCADE, cell, CELLS, Cells, Cultured, Cellular, Cerebellar, cerebellum, Clone Cells, control, cytology, DELETION, dendrite, dendrites, depression, DETERMINANT, Disruption, Electric Stimulation, electrophysiology, EXAMPLE, Extremities, EYE MOVEMENTS, Form, function, genetic, genetics, glutamate, IM, IMPAIRMENT, in vitro, integration, LA, Locomotion, LONG-TERM, Long-Term Depression (Physiology), May, metabolism, Methods, mice, Mice, Inbred C57BL, Mutant Strains, Microscopy, Video, Mutant, Patch-Clamp Techniques, physiology, PROTEIN, Purkinje cell, Purkinje cells, RELEVANT, Result, sensory, signal, SPINE, Stem Cells, Stimulation, Support, Non-U.S.Gov't, Synapses, synaptic transmission, TIME, transmission, vitamin |
| UCL classification: | UCL UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Brain Sciences UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Brain Sciences > UCL Queen Square Institute of Neurology UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Brain Sciences > UCL Queen Square Institute of Neurology > UK Dementia Research Institute |
| URI: | https://discovery.ucl.ac.uk/id/eprint/172499 |
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