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Modulation of the glycine response by Ca 2+ ‐permeable AMPA receptors in rat spinal neurones
Author(s) -
Xu TianLe,
Li JiShuo,
Jin YoungHo,
Akaike Norio
Publication year - 1999
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.1469-7793.1999.701ad.x
Subject(s) - ampa receptor , chemistry , long term potentiation , kainate receptor , postsynaptic potential , biophysics , nmda receptor , glycine receptor , bapta , inhibitory postsynaptic potential , receptor , glycine , neuroscience , biochemistry , biology , amino acid
1 In acutely isolated rat sacral dorsal commisural nucleus (SDCN) neurones, application of kainate (KA) reversibly potentiated glycine‐evoked Cl − currents ( I Gly ) in a concentration‐dependent manner. 2 The cellular events underlying the interaction between non‐NMDA receptors and glycine receptors were studied by using nystatin‐perforated patch and cell‐attached single‐channel recording modes. 3 The action of KA was not accompanied by a shift in the reversal potential for I Gly . In dose‐response curves, KA potentiated I Gly without significantly changing glycine binding affinity. 4 GYKI 52466 blocked while NS‐102 had no effect on the KA‐induced potentiation of I Gly . 5 The potentiation was reduced when KA was applied in a Ca 2+ ‐free extracellular solution or in the presence of BAPTA AM, and was independent of the activation of voltage‐dependent Ca 2+ channels. 6 Pretreatment with KN‐62, a selective Ca 2+ ‐calmodulin‐dependent protein kinase II (CaMKII) inhibitor, abolished the action of KA. Inhibition of calcineurin converted the KA‐induced potentiation to a sustained one. 7 Single‐channel recordings revealed that KA decreased the mean closing time of glycine‐gated single‐channel activity, resulting in an increase in the probability of channel opening. 8 It is proposed that Ca 2+ entry through AMPA receptors modulates the glycine receptor function via coactivation of CaMKII and calcineurin in SDCN neurones. This interaction may provide a new postsynaptic mechanism for control of inhibitory synaptic signalling and represent one of the important regulatory mechanisms of spinal nociception.