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Presynaptic kainate receptor‐mediated facilitation of glutamate release involves Ca 2+ –calmodulin and PKA in cerebrocortical synaptosomes
Author(s) -
Rodríguez-Moreno Antonio,
Sihra Talvinder S.
Publication year - 2013
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2013.01.071
Subject(s) - kainate receptor , glutamate receptor , facilitation , chemistry , nbqx , ampa receptor , calmodulin , biophysics , nmda receptor , biochemistry , neuroscience , receptor , biology , enzyme
We have explored the mechanisms involved in the facilitation of glutamate release mediated by the activation of kainate receptors (KARs) in the cortex using isolated nerve terminals (synaptosomes). Kainate (KA) produced an increase on glutamate release at 100 μM. The effect of KA was antagonized by NBQX (with AMPA receptors blocked by GYKI53655). This facilitation was suppressed by the inhibition of PKA activation by Rp‐Br‐cAMP and H‐89. Moreover, the facilitation of glutamate release mediated by KAR requires the mobilization of intrasynaptosomal Ca 2+ stores and the formation of a Ca 2+ –calmodulin complex. We conclude that KARs present on presynaptic terminals in the neocortex mediate the facilitation of glutamate release through a mechanism involving an increase in cytosolic Ca 2+ to activate a Ca 2+ –calmodulin–AC/cAMP/PKA signaling cascade.