The conundrum of sensitization when recording from nociceptors

Mer fra Geoffrey Bove om nervogene betenneler og nocicepsjon. Denne forholder seg til nocicepsjon som oppstår under måling av nocicepsjon i studier, men har mange interessante poenger. Nevner at noceceptiv sensitering og kontinuerlig nociceptive aktivitet (ongoing activity(OA)) skjer spesielt i betennelsestilstander. Dette er grunnen til at alle med betennelsestilstander i kroppen bør senke betennelsesnivå for å få resultater av behandling.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2854223/

When sensitized, nociceptors often exhibit activity in the absence of apparent or additional stimulation, called ongoing (or spontaneous) activity (OA).

We suggest that there are two types of OA, characterized by their rates. Very slow rates of ongoing activity (<0.2 Hz) are likely to arise from the receptive field and may indicate sensitization during the experiment. Faster rates are likely to arise from the nerve trunk, i.e. the neuritis, or the neuronal cell body.

A key feature of nociceptors is that they develop ongoing activity (OA) when they, or the structures they innervate, are injured or inflamed (Bessou and Perl, 1969Perl, 1976Perl, Kumazawa et al., 1976).

To locate RFs, especially in deep tissues, the structures must be stimulated noxiously. Thus, when a slowly conducting neuron is isolated, the peripheral structures from the distal thigh to the toes are stimulated noxiously using fingers or forceps. However, if a mechanical receptive field is not found, another neuron is isolated, and the search repeated. This typically takes dozens of searches over the course of the recording sessions, which in these experiments were 4–7 hours long. In our experiments it was clear that the noxious mechanical stimulus necessary to identify the RFs was in itself sufficient to cause inflammation.

Ongoing activity in sensory elements could be expected to impact the sensory modality of that element. Thus, OA in nociceptors could be expected to lead to the sensation of pain. However, the discharge rate that is necessary to reach perception remains unclear, and definitive studies have not been performed.

Using microneurography in humans, which is similar to the methods reported here, Konietzny et al., reported that electrically evoked nociceptor discharge rates as low at 0.5 Hz could evoke pain (Konietzny, Perl et al., 1981). Another human study reported that while nociceptor discharge under 0.2 Hz usually did not evoke pain, 0.4 Hz usually did (Van Hees and Gybels, 1981), consistent with a similar report (Van Hees and Gybels, 1972). These findings are in general consistent with our findings (Fig. 3). Although it thus remains unknown whether very slow levels of OA are significant for pain, any low rate will release neurotransmitters at their synapses in the spinal cord, which may be extensive due to the high degree of branching of primary afferent neurons to spinal cord neurons.

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