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Kainate receptor‐mediated depression of glutamatergic transmission involving protein kinase A in the lateral amygdala
Author(s) -
NegreteDíaz José Vicente,
DuqueFeria Paloma,
AndradeTalavera Yuniesky,
Carrión Miriam,
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.1471-4159.2012.07665.x
Subject(s) - kainate receptor , neuroscience , excitatory postsynaptic potential , neurotransmission , postsynaptic potential , glutamatergic , postsynaptic current , chemistry , glutamate receptor , biophysics , biology , microbiology and biotechnology , receptor , ampa receptor , inhibitory postsynaptic potential , biochemistry
J. Neurochem. (2012) 121 , 36–43. Abstract Kainate receptors (KARs) have been described as modulators of synaptic transmission at different synapses. However, this role of KARs has not been well characterized in the amygdala. We have explored the effect of kainate receptor activation at the synapse established between fibers originating at medial geniculate nucleus and the principal cells in the lateral amygdala. We have observed an inhibition of evoked excitatory postsynaptic currents (eEPSCs) amplitude after a brief application of KARs agonists KA and ATPA. Paired‐pulse recordings showed a clear pair pulse facilitation that was enhanced after KA or ATPA application. When postsynaptic cells were loaded with BAPTA, the depression of eEPSC amplitude observed after the perfusion of KAR agonists was not prevented. We have also observed that the inhibition of the eEPSCs by KARs agonists was prevented by protein kinase A but not by protein kinase C inhibitors. Taken together our results indicate that KARs present at this synapse are pre‐synaptic and their activation mediate the inhibition of glutamate release through a mechanism that involves the activation of protein kinase A.