Kainate receptor-mediated depression of glutamatergic transmission involving protein kinase A in the lateral amygdala

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 m...

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Detalles Bibliográficos
Autores: Negrete Diaz, Jose Vicente, Duque Feria, Paloma, Andrade Talavera, Yuniesky, Carrión Reinoso, Miriam, Flores Álvarez, Gonzalo, Rodríguez-Moreno, Antonio
Tipo de recurso: artículo
Fecha de publicación:2012
País:España
Institución:Universidad Pablo de Olavide (UPO)
Repositorio:RIO. Repositorio Institucional Olavide
Idioma:inglés
OAI Identifier:oai:rio.upo.es:10433/23672
Acceso en línea:https://hdl.handle.net/10433/23672
Access Level:acceso abierto
Palabra clave:Amygdala
Glutamate
Kainate receptors
Pre-synaptic
Protein kinase A
Descripción
Sumario: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.