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Elevation of intradendritic sodium concentration mediated by synaptic activation of metabotropic glutamate receptors in cerebellar Purkinje cells
Author(s) -
Knöpfel T.,
Anchisi D.,
Alojado M. E.,
Tempia F.,
Strata P.
Publication year - 2000
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1046/j.1460-9568.2000.00122.x
Subject(s) - metabotropic glutamate receptor , metabotropic glutamate receptor 1 , neuroscience , metabotropic glutamate receptor 5 , chemistry , glutamate receptor , metabotropic receptor , metabotropic glutamate receptor 6 , metabotropic glutamate receptor 7 , metabotropic glutamate receptor 2 , long term depression , metabotropic glutamate receptor 4 , receptor , biology , biochemistry , ampa receptor
Cerebellar Purkinje cells express both ionotropic glutamate receptors and metabotropic glutamate receptors. Brief tetanic stimulation of parallel fibers in rat and mouse cerebellar slices evokes a slow excitatory postsynaptic current in Purkinje cells that is mediated by the mGluR 1 subtype of metabotropic glutamate receptors. The effector system underlying this mGluR 1 EPSC has not yet been identified. In the present study, we recorded the mGluR 1 EPSC using the whole‐cell patch‐clamp technique in combination with microfluorometric recordings of the intracellular sodium concentration ([Na + ] i ) by means of the fluorescent sodium indicator SBFI. The mGluR 1 EPSC was induced by local parallel fibre stimulation in the presence of the ionotropic glutamate receptor antagonists NBQX and D‐APV and the GABA A receptor antagonists bicuculline or picrotoxin. The mGluR 1 EPSC was associated with an increase in [Na + ] i that was restricted to a specific portion of the dendritic tree. The mGluR 1 EPSC as well as the increase in [Na + ] i were inhibited by the mGluR antagonist S‐MCPG. In the presence of NBQX, D‐APV, pictrotoxin and TTX, bath application of the selective mGluR agonist 3,5‐DHPG induced an elevation in [Na + ] i which extended over the whole dendritic field of the Purkinje cell. This finding demonstrates that the mGluR 1 ‐mediated postsynaptic current leads to a significant influx of sodium into the dendritic cytoplasm of Purkinje cells and thereby provides a novel intracellular signalling mechanism that might be involved in mGluR 1 ‐dependent synaptic plasticity at this synapse.