Interneuron- and GABAA receptor-specific inhibitory synaptic plasticity in cerebellar Purkinje cells

Qionger He, Ian Duguid, Beverley Clark, Patrizia Panzanelli, Bijal Patel, Philip Thomas, Jean-Marc Fritschy and Trevor G. Smart ()
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Qionger He: Physiology and Pharmacology, UCL
Ian Duguid: Physiology and Pharmacology, UCL
Beverley Clark: Wolfson Institute for Biomedical Research, UCL
Patrizia Panzanelli: University of Turin
Bijal Patel: Physiology and Pharmacology, UCL
Philip Thomas: Physiology and Pharmacology, UCL
Jean-Marc Fritschy: Institute of Pharmacology, University of Zurich
Trevor G. Smart: Physiology and Pharmacology, UCL

Nature Communications, 2015, vol. 6, issue 1, 1-13

Abstract: Abstract Inhibitory synaptic plasticity is important for shaping both neuronal excitability and network activity. Here we investigate the input and GABAA receptor subunit specificity of inhibitory synaptic plasticity by studying cerebellar interneuron–Purkinje cell (PC) synapses. Depolarizing PCs initiated a long-lasting increase in GABA-mediated synaptic currents. By stimulating individual interneurons, this plasticity was observed at somatodendritic basket cell synapses, but not at distal dendritic stellate cell synapses. Basket cell synapses predominantly express β2-subunit-containing GABAA receptors; deletion of the β2-subunit ablates this plasticity, demonstrating its reliance on GABAA receptor subunit composition. The increase in synaptic currents is dependent upon an increase in newly synthesized cell surface synaptic GABAA receptors and is abolished by preventing CaMKII phosphorylation of GABAA receptors. Our results reveal a novel GABAA receptor subunit- and input-specific form of inhibitory synaptic plasticity that regulates the temporal firing pattern of the principal output cells of the cerebellum.

Date: 2015
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DOI: 10.1038/ncomms8364

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