|
KMID : 0948920020010010005
|
|
Clinical Pain
2002 Volume.1 No. 1 p.5 ~ p.8
|
|
|
Physiology of Pain in Clinical Practice
|
|
Kim Sang-Jung
|
|
|
Abstract
|
|
|
|
Pain is defined as an unpleasant sensory and emotional experience associated with actual or potential tissue damage (International Association for the Study of Pain, 1979), and may be classified as initial pain and delayed pain according to temporal characteristics. Pain is mediated to the central nervous system through pathways involving nociceptors, pain- transmitting Aδ- and C-fibers, the dorsal root ganglion (DRG), structures in the dorsal horn and numerous main-mediating substances. Hyperalgesia is the increased sensitivity to pain in response to nonpainful stimuli following peripheral tissue injury. It is mediated by repetitive firing of C-fibers leading to increased sensitivity of substantia gelatinosa neurons (SGN) to painful stimuli. This SGN potentiation is in turn due to the long term potentiation (LTP) originating from the excitatory postsynaptic potential (EPSP) generated by the neurotransmitter glutamate in response to high-frequency C-fiber activation. Further research is underway regarding the mechanism of long term potentiation in the SGN.
|
|
|
KEYWORD
|
|
|
Pain, Nociceptor, Substantia gelatinosa, Long term potentiation
|
|
|
FullTexts / Linksout information
|
|
|
|
|
Listed journal information
|
|
|
|