Cellular and Molecular Mechanisms of Pain

Denne beskriver det aller meste om nociceptorer. Jeg biter meg merke i det siste avsnittet som beskriver noe av årsaken til at det ikke er så enkelt som å kallen en nociceptor for smertereseptor. De avslutter med å si at studier av nocicepsjon kan bane vei for å forstå kronisk smerte, men av forrige blog jeg la ut forstår vi at i hjernen er det en tydelig forskjell mellom kronisk og akutt smerte. Så åpenbart er det helt andre mekanismer som ligger til grunn.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2852643/

These observations argue for behaviorally-relevant specificity at the level of the nociceptor. However, this is likely to be an oversimplification for at least two reasons. First, many nociceptors are polymodal and can therefore be activated by thermal, mechanical, or chemical stimuli, leaving one to wonder how elimination of large cohorts of nociceptors can have modality-specific effects. This argues for a substantial contribution of spinal circuits to the process whereby nociceptive signals are encoded into distinct pain modalities. Indeed, an important future goal is to better delineate neuronal subtypes within the dorsal horn and characterize their synaptic interactions with functionally or molecularly defined subpopulations of nociceptors. Second, the pain system shows a tremendous capacity for change, particularly in the setting of injury, raising questions about whether and how a labeled line system might accommodate such plasticity, and how alterations in such mechanisms underlie maladaptive changes that produce chronic pain. Indeed, we know that substance P-saporin-mediated deletion of a discrete population of lamina I dorsal horn neurons, which express the substance P receptor, can reduce both the thermal and mechanical pain hypersensitivity that occurs after tissue or nerve injury (Nichols et al., 1999). Such observations suggest that in the setting of injury specificity of the labeled line is not strictly maintained as information is transmitted to higher levels of the neuraxis.

Doing so should bring us closer to understanding how acute pain gives way to the maladaptive changes that produce chronic pain, and how this switch can be prevented or reversed.

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