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Regulation of kainate receptors by protein kinase C and metabotropic glutamate receptors
Author(s) -
Cho Kwangwook,
Francis Joanna C.,
Hirbec Hélène,
Dev Kumlesh,
Brown Malcolm W.,
Henley Jeremy M.,
Bashir Zafar I.
Publication year - 2003
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1111/j.1469-7793.2003.00723.x
Subject(s) - kainate receptor , metabotropic glutamate receptor , long term depression , class c gpcr , synaptic plasticity , metabotropic glutamate receptor 6 , metabotropic glutamate receptor 5 , metabotropic glutamate receptor 7 , metabotropic receptor , neuroscience , metabotropic glutamate receptor 2 , biology , neurotransmission , ion channel linked receptors , metabotropic glutamate receptor 3 , glutamate receptor , microbiology and biotechnology , chemistry , receptor , ampa receptor , biochemistry
Kainate receptors have recently been shown to be involved in synaptic transmission, to regulate transmitter release and to mediate synaptic plasticity in different regions of the CNS. However, very little is known about endogenous mechanisms that can control native kainate receptor signalling. In this study we have found that GluR5‐containing kainate receptor‐mediated actions can be modulated by activation of protein kinase C (PKC) but not protein kinase A (PKA). However, both PKA and PKC directly phosphorylate the GluR5 subunit of kainate receptors. Metabotropic glutamate (mGlu) receptors are well known to be involved in synaptic transmission, regulation of transmitter release and synaptic plasticity in a variety of brain regions. We now demonstrate that kainate receptor signalling is enhanced by activation of group I mGlu receptors, in a PKC‐dependent manner. These data demonstrate for the first time that kainate receptor function can be modulated by activation of metabotropic glutamate receptors and have implications for understanding mechanisms of synaptic transmission, plasticity and disorders such as epilepsy.