Presynaptic kainate receptor-mediated facilitation of glutamate release involves Ca2+-calmodulin and PKA in cerebrocortical synaptosomes.

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.

journal_name

FEBS Lett

journal_title

FEBS letters

authors

Rodríguez-Moreno A,Sihra TS

doi

10.1016/j.febslet.2013.01.071

subject

Has Abstract

pub_date

2013-03-18 00:00:00

pages

788-92

issue

6

eissn

0014-5793

issn

1873-3468

pii

S0014-5793(13)00118-X

journal_volume

587

pub_type

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