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Ca 2+ ‐dependent regulation of synaptic δ2 glutamate receptor density in cultured rat Purkinje neurons
Author(s) -
Hirai Hirokazu
Publication year - 2001
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.0953-816x.2001.01630.x
Subject(s) - synaptogenesis , glutamatergic , synaptic plasticity , glutamate receptor , postsynaptic density , postsynaptic potential , neuroscience , biology , nmda receptor , metabotropic glutamate receptor , excitatory postsynaptic potential , long term depression , microbiology and biotechnology , receptor , ampa receptor , inhibitory postsynaptic potential , biochemistry
The δ2 glutamate receptor (δ2 receptor), which is expressed abundantly at parallel fibre–Purkinje neuron synapses, has an important role in synaptogenesis and synaptic plasticity in the cerebellum. The present study examined the molecular mechanisms regulating synaptic δ2 receptor density. Immunocytochemistry, using two antibodies against the intracellular C‐terminal and extracellular N‐terminal regions of the δ2 receptor, indicated the reversible redistribution of postsynaptic δ2 receptors in response to either glutamatergic stimulation or enhancement of synaptic activity. The effect of glutamatergic stimulation was completely inhibited by either coapplication of the glutamate receptor antagonist or the removal of extracellular Ca 2+ using EGTA and mimicked by selective activation of voltage‐gated Ca 2+ channels (VGCCs) with KCl, suggesting the significant role of Ca 2+ influx in δ2 receptor redistribution. Biochemical examination indicated that a large amount of δ2 receptor protein was internalized following glutamatergic stimulation. These results suggest that the number of synaptic δ2 receptors is controlled by endocytosis in a synaptic activity‐ and intracellular Ca 2+ ‐dependent way, through which synaptogenesis and synaptic plasticity in Purkinje cells might be modulated.