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Presynaptic kainate receptor‐mediated facilitation of glutamate release involves Ca 2+ –calmodulin at mossy fiber–CA3 synapses
Author(s) -
AndradeTalavera Yuniesky,
DuqueFeria Paloma,
NegreteDíaz José Vicente,
Sihra Talvinder S.,
Flores Gonzalo,
RodríguezMoreno Antonio
Publication year - 2012
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.2012.07844.x
Subject(s) - glutamate receptor , kainate receptor , calmodulin , neurotransmitter , biophysics , chemistry , biology , neuroscience , biochemistry , microbiology and biotechnology , receptor , ampa receptor , enzyme
J. Neurochem . (2012) 122 , 891–899. Abstract Presynaptic kainate receptors (KARs) modulate the release of glutamate at synapses established between mossy fibers (MF) and CA3 pyramidal cells in the hippocampus. The activation of KAR by low, nanomolar, kainate concentrations facilitates glutamate release. KAR‐mediated facilitation of glutamate release involves the activation of an adenylate cyclase/cyclic adenosine monophosphate/protein kinase A cascade at MF–CA3 synapses. Here, we studied the mechanisms by which KAR activation produces this facilitation of glutamate release in slices and synaptosomes. We find that the facilitation of glutamate release mediated by KAR activation requires an increase in Ca 2+ levels in the cytosol and the formation of a Ca 2+ –calmodulin complex to activate adenylate cyclase. The increase in cytosolic Ca 2+ underpinning this modulation is achieved, both, by Ca 2+ entering via Ca 2+ ‐permeable KARs and, by the mobilization of intraterminal Ca 2+ stores. Finally, we find that, congruent with the Ca 2+ –calmodulin support of KAR‐mediated facilitation of glutamate release, induction of long‐term potentiation at MF–CA3 synapses has an obligate requirement for Ca 2+ –calmodulin activity.