Differential GABAergic and glycinergic inputs of inhibitory interneurons and Purkinje cells to principal cells of the cerebellar nuclei.
Journal of Neuroscience. 2014-07-09; 34(28): 9418-9431
DOI: 10.1523/JNEUROSCI.0401-14.2014
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1. J Neurosci. 2014 Jul 9;34(28):9418-31. doi: 10.1523/JNEUROSCI.0401-14.2014.
Husson Z(1), Rousseau CV(1), Broll I(2), Zeilhofer HU(3), Dieudonné S(4).
Author information:
(1)Ecole Normale Supérieure, Institut de Biologie de l’ENS (IBENS), Inserm U1024, and CNRS UMR 8197, F-75005 Paris, France.
(2)Institute of Pharmacology and Toxicology, University of Zurich, CH-8057 Zürich, Switzerland, and.
(3)Institute of Pharmaceutical Sciences, Swiss Federal Institute of Technology (ETH Zürich), CH-8090 Zürich, Switzerland.
(4)Ecole Normale Supérieure, Institut de Biologie de l’ENS (IBENS), Inserm U1024, and CNRS UMR 8197, F-75005 Paris, France.
The principal neurons of the cerebellar nuclei (CN), the sole output of the olivo-cerebellar system, receive a massive inhibitory input from Purkinje cells (PCs) of the cerebellar cortex. Morphological evidence suggests that CN principal cells are also contacted by inhibitory interneurons, but the properties of this connection are unknown. Using transgenic, tracing, and immunohistochemical approaches in mice, we show that CN interneurons form a large heterogeneous population with GABA/glycinergic phenotypes, distinct from GABAergic
olive-projecting neurons. CN interneurons are found to contact principal output neurons, via glycine receptor (GlyR)-enriched synapses, virtually devoid of the main GABA receptor (GABAR) subunits α1 and γ2. Those clusters account for 5% of the total number of inhibitory receptor clusters on principal neurons. Brief optogenetic stimulations of CN interneurons, through selective expression ofchannel rhodopsin 2 after viral-mediated transfection of the flexed gene in GlyT2-Cre transgenic mice, evoked fast IPSCs in principal cells. GlyR activation
accounted for 15% of interneuron IPSC amplitude, while the remaining current was mediated by activation of GABAR. Surprisingly, small GlyR clusters were also found at PC synapses onto principal CN neurons in addition to α1 and γ2 GABAR subunits. However, GlyR activation was found to account for