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Synaptic plasticity in chronic pain
Author(s) -
Zieglgänsberger W.
Publication year - 2003
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.85.s2.12_2.x
Subject(s) - neuroscience , endocannabinoid system , extinction (optical mineralogy) , amygdala , inhibitory postsynaptic potential , synaptic plasticity , chronic pain , psychology , biology , receptor , paleontology , biochemistry
Chronic pain syndromes are characterized by altered neuronal excitability in the pain matrix. These long‐term changes most commonly require alterations in gene expression. Immediate‐early genes (IEGs) are thought to participate as third messengers in the late phase of the stimulus transcription cascade in neurons of the pain matrix. The ability to rapidly acquire and store memory of aversive events is one of the basic principles of central nervous systems throughout the animal kingdom. In the absence of reinforcement the resulting behavioral response of the organism will gradually diminish to be finally extinct. The cellular mechanisms of extinction are largely unknown. The endogenous cannabinoid system plays a central role in the extinction of aversive memories. We proposed that endocannabinoids facilitate extinction of aversive memories via their selective inhibitory effects on GABAergic networks in the amygdala (1).