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Philos Trans R Soc Lond B Biol Sci. 2013 Dec 2;369(1633):20130146. doi: 10.1098/rstb.2013.0146. Print 2014 Jan 5.

Long-term potentiation in the anterior cingulate cortex and chronic pain.

Author information

1
Center for Neuron and Disease, Frontier Institutes of Life Science, Science and Technology, Xi'an Jiaotong University, , Xi'an 710049, People's Republic of China.

Abstract

Glutamate is the primary excitatory transmitter of sensory transmission and perception in the central nervous system. Painful or noxious stimuli from the periphery 'teach' humans and animals to avoid potentially dangerous objects or environments, whereas tissue injury itself causes unnecessary chronic pain that can even last for long periods of time. Conventional pain medicines often fail to control chronic pain. Recent neurobiological studies suggest that synaptic plasticity taking place in sensory pathways, from spinal dorsal horn to cortical areas, contributes to chronic pain. Injuries trigger long-term potentiation of synaptic transmission in the spinal cord dorsal horn and anterior cingulate cortex, and such persistent potentiation does not require continuous neuronal activity from the periphery. At the synaptic level, potentiation of excitatory transmission caused by injuries may be mediated by the enhancement of glutamate release from presynaptic terminals and potentiated postsynaptic responses of AMPA receptors. Preventing, 'erasing' or reducing such potentiation may serve as a new mechanism to inhibit chronic pain in patients in the future.

KEYWORDS:

adenylyl cyclase; analgesia; anterior cingulate cortex; chronic pain; cyclic adenosine monophosphate; long-term potentiation

PMID:
24298148
PMCID:
PMC3843878
DOI:
10.1098/rstb.2013.0146
[Indexed for MEDLINE]
Free PMC Article

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