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Updated: May 14, 2026

Fast Micro-iontophoresis of Glutamate and GABA: A Useful Tool to Investigate Synaptic Integration
Published on: July 31, 2013
Presynaptic kainate receptor-mediated facilitation of glutamate release involves Ca2+-calmodulin and PKA in
Antonio Rodríguez-Moreno1, Talvinder S Sihra
1Laboratory of Cellular Neuroscience and Plasticity, Department of Physiology, Anatomy and Cellular Biology, University Pablo de Olavide, Seville, Spain. arodmor@upo.es
Abstract:
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.
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