4.5 Article

Kainate receptor modulation of glutamatergic synaptic transmission in the CA2 region of the hippocampus

期刊

JOURNAL OF NEUROCHEMISTRY
卷 158, 期 5, 页码 1083-1093

出版社

WILEY
DOI: 10.1111/jnc.15481

关键词

CA2; G protein; GluK1; glutamate; hippocampus; kainate receptor; protein kinase A

资金

  1. Agencia Estatal de Investigacion
  2. FEDER [BFU2015-68655-P]
  3. Universidad Pablo de Olavide/ CBUA

向作者/读者索取更多资源

KARs in the CA2 region of the hippocampus mediate the depression of glutamate release through a mechanism involving the activation of G protein and protein kinase A.
Kainate (KA) receptors (KARs) are important modulators of synaptic transmission. We studied here the role of KARs on glutamatergic synaptic transmission in the CA2 region of the hippocampus where the actions of these receptors are unknown. We observed that KA depresses glutamatergic synaptic transmission at Schaffer collateral-CA2 synapses; an effect that was antagonized by NBQX (a KA/AMPA receptors antagonist) under condition where AMPA receptors were previously blocked. The study of paired-pulse facilitation ratio, miniature responses, and fluctuation analysis indicated a presynaptic locus of action for KAR. Additionally, we determined the action mechanism for this depression of glutamate release mediated by the activation of KARs. We found that inhibition of protein kinase A suppressed the effect of KAR activation on evoked excitatory post-synaptic current, an effect that was not suppressed by protein kinase C inhibitors. Furthermore, in the presence of Pertussis toxin, the depression of glutamate release mediated by KAR activation was not present, invoking the participation of a G(i/o) protein in this modulation. Finally, the KAR-mediated depression of glutamate release was not suppressed by treatments that affect calcium entry trough voltage-dependent calcium channels or calcium release from intracellular stores. We conclude that KARs present at these synapses mediate a depression of glutamate release through a mechanism that involves the activation of G protein and protein kinase A.

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