Presynaptic long-term potentiation requires extracellular signal-regulated kinases in the anterior cingulate cortex

Extracellular signal-regulated kinases are widely expressed protein kinases in neurons, which serve as important intracellular signaling molecules for central plasticity such as long-term potentiation. Recent studies demonstrate that there are two major forms of long-term potentiation in cortical ar...

Full description

Saved in:
Bibliographic Details
Published in:Molecular Pain 2020, Vol.16, p.1744806920917245-1744806920917245
Main Authors: Chen, Qi-Yu, Zhang, Zhi-Ling, Liu, Qin, Chen, Chao-Jun, Zhang, Xiao-Kang, Xu, Ping-Yi, Zhuo, Min
Format: Article
Language:English
Subjects:
Acute Pain - drug therapy
Animals
Chronic pain
Chronic Pain - drug therapy
Cortex (cingulate)
Excitatory Postsynaptic Potentials
Extracellular Signal-Regulated MAP Kinases - metabolism
Gyrus Cinguli - metabolism
Hippocampus - metabolism
Humans
Intracellular signalling
Learning
Long-Term Potentiation
MAP Kinase Signaling System
Molecular modelling
Neurons - metabolism
Presynaptic Terminals - metabolism
Protein kinase
Review
Signal Transduction
Synapses - metabolism
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Extracellular signal-regulated kinases are widely expressed protein kinases in neurons, which serve as important intracellular signaling molecules for central plasticity such as long-term potentiation. Recent studies demonstrate that there are two major forms of long-term potentiation in cortical areas related to pain: postsynaptic long-term potentiation and presynaptic long-term potentiation. In particular, presynaptic long-term potentiation in the anterior cingulate cortex has been shown to contribute to chronic pain-related anxiety. In this review, we briefly summarized the components and roles of extracellular signal-regulated kinases in neuronal signaling, especially in the presynaptic long-term potentiation of anterior cingulate cortex, and discuss the possible molecular mechanisms and functional implications in pain-related emotional disorders.
ISSN:1744-8069
1744-8069
DOI:10.1177/1744806920917245