[Molecular mechanisms in acute and chronic pain states].
BACKGROUND
Pain is a sense necessary for survival and has a complex neurobiological basis. In recent years a powerful battery of techniques has been developed to unravel the mechanisms by which painful stimuli are transduced and processed both in the acute and pathological state.
We review the literature with special emphasis on recent discoveries regarding the molecular transduction mechanisms in nociceptors and novel molecular and cellular mechanisms underlying the spinal processing of painful stimuli.


CONCLUSIONS
The mechanisms by which sensory neurons initiate hyperalgesia and touch-evoked pain (allodynia) have been addressed particularly successfully in recent studies. The rich variety of key molecular players that have emerged in physiological and pathophysiological pain states reflects the sophistication and uniqueness of this important sense. This is good news for both the pain scientist and the pain clinician since it increases the intellectual challenge and provides a plethora of targets for novel analgesics and treatments.
Rygh
Lars Jørgen
LJ
Institutt for biomedisin, Seksjon for fysiologi, Universitetet i Bergen, Jonas Lies vei 91, 5009 Bergen. lars.jorgen.rygh@biomed.uib.no
Hole
Kjell
K
Tjølsen
Arne
A
D000208:Acute Disease; D000698:Analgesia; D000700:Analgesics / Q000627:therapeutic use; D002908:Chronic Disease; D006801:Humans; D009473:Neuronal Plasticity / Q000502:physiology; D009475:Neurons, Afferent / Q000502:physiology; D009619:Nociceptors / Q000378:metabolism / Q000502:physiology*; D010146:Pain / Q000378:metabolism / Q000503:physiopathology*; D059408:Pain Management; D016194:Receptors, N-Methyl-D-Aspartate / Q000502:physiology; D015398:Signal Transduction / Q000502:physiology
D000700:Analgesics; D016194:Receptors, N-Methyl-D-Aspartate