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Mechanisms underlying excitatory effects of group I metabotropic glutamate receptors via inhibition of 2P domain K + channels
Author(s) -
Chemin Jean,
Girard Christophe,
Duprat Fabrice,
Lesage Florian,
Romey Georges,
Lazdunski Michel
Publication year - 2003
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1093/emboj/cdg528
Subject(s) - biology , metabotropic glutamate receptor , excitatory postsynaptic potential , metabotropic glutamate receptor 2 , metabotropic glutamate receptor 4 , metabotropic glutamate receptor 5 , glutamate receptor , metabotropic glutamate receptor 6 , metabotropic glutamate receptor 3 , metabotropic receptor , metabotropic glutamate receptor 8 , metabotropic glutamate receptor 1 , neuroscience , metabotropic glutamate receptor 7 , biophysics , receptor , biochemistry
Group I metabotropic glutamate receptors (mGluRs) are implicated in diverse processes such as learning, memory, epilepsy, pain and neuronal death. By inhibiting background K + channels, group I mGluRs mediate slow and long‐lasting excitation. The main neuronal representatives of this K + channel family (K 2P or KCNK) are TASK and TREK. Here, we show that in cerebellar granule cells and in heterologous expression systems, activation of group I mGluRs inhibits TASK and TREK channels. D ‐ myo ‐inositol‐1,4,5‐triphosphate and phosphatidyl‐4,5‐inositol‐biphosphate depletion are involved in TASK channel inhibition, whereas diacylglycerols and phosphatidic acids directly inhibit TREK channels. Mechanisms described here with group I mGluRs will also probably stand for many other receptors of hormones and neurotransmitters.