Vagus Nerve Stimulation Enhances Extinction of Conditioned Fear in Rats and Modulates Arc Protein, CaMKII, and GluN2B-Containing NMDA Receptors in the Basolateral Amygdala

Vagus nerve stimulation (VNS) enhances the consolidation of extinction of conditioned fear. High frequency stimulation of the infralimbic cortex (IL) produces long-term potentiation in the basolateral amygdala (BLA) in rats given VNS-paired extinction training, whereas the same stimulation produces...

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Veröffentlicht in:Neural plasticity. - 1998. - 2016(2016) vom: 26., Seite 4273280
1. Verfasser: Alvarez-Dieppa, Amanda C (VerfasserIn)
Weitere Verfasser: Griffin, Kimberly, Cavalier, Sheridan, McIntyre, Christa K
Format: Online-Aufsatz
Sprache:English
Veröffentlicht: 2016
Zugriff auf das übergeordnete Werk:Neural plasticity
Schlagworte:Journal Article Cytoskeletal Proteins Excitatory Amino Acid Antagonists NR2B NMDA receptor Nerve Tissue Proteins Receptors, N-Methyl-D-Aspartate activity regulated cytoskeletal-associated protein Calcium-Calmodulin-Dependent Protein Kinase Type 2 EC 2.7.11.17
Beschreibung
Zusammenfassung:Vagus nerve stimulation (VNS) enhances the consolidation of extinction of conditioned fear. High frequency stimulation of the infralimbic cortex (IL) produces long-term potentiation in the basolateral amygdala (BLA) in rats given VNS-paired extinction training, whereas the same stimulation produces long-term depression in sham-treated rats. The present study investigated the state of synaptic plasticity-associated proteins in the BLA that could be responsible for this shift. Male Sprague-Dawley rats were separated into 4 groups: auditory fear conditioning only (fear-conditioned); fear conditioning + 20 extinction trials (extended-extinction); fear conditioning + 4 extinction trials paired with sham stimulation (sham-extinction); fear conditioning + 4 extinction trials paired with VNS (VNS-extinction). Freezing was significantly reduced in extended-extinction and VNS-extinction rats. Western blots were used to quantify expression and phosphorylation state of synaptic plasticity-associated proteins such as Arc, CaMKII, ERK, PKA, and AMPA and NMDA receptors. Results show significant increases in GluN2B expression and phosphorylated CaMKII in BLA samples from VNS- and extended-extinction rats. Arc expression was significantly reduced in VNS-extinction rats compared to all groups. Administration of the GluN2B antagonist ifenprodil immediately after fear extinction training blocked consolidation of extinction learning. Results indicate a role for BLA CaMKII-induced GluN2B expression and reduced Arc protein in VNS-enhanced extinction
Beschreibung:Date Completed 29.08.2017
Date Revised 10.03.2022
published: Print-Electronic
Citation Status MEDLINE
ISSN:1687-5443