The authors of these articles [Maihofner et al., 2007: (http://www.ncbi.nlm.nih.gov/pubmed/17767511); Seifert et al., 2008: (http://www.ncbi.nlm.nih.gov/pubmed/17948883)] performed MRI's on UVB-exposed humans and found augmentations of nociceptive responses, to various stimuli, in different parts of the brain. That doesn't provide definitve evidence of central sensitization or central effects, technically, because secondary mechanical and thermal hyperalgesia and allodynia can all be mediated by peripheral mechanisms. For example, more CGRP and SP might be released from the central terminals of C-type dorsal root ganglion (DRG) neurons per incoming action potential, or there might be some other change in the DRG neurons. There are almost certainly central components to UVB-induced allodynia (nociceptive responses to innocuous, peripheral, mechanical stimuli) and secondary mechanical hyperalgesia (enlargement of the receptive fields of some dorsal horn (DH) neurons, so that nociceptive responses can be elicited by mechanical stimuli that are applied outside the irradiated skin site), though, because the augmentation of nociceptive transmission, in the DH, in response to mechanoreceptive inputs, from outside the irradiated site, is likely to occur through heterosynaptic facilitation in the DH. UV exposure induces spontaneous action potentials (AP's) in C-fibers and Adelta-fibers that form synapses with DH neurons in one or another part of the DH, and the Abeta-type DRG neurons that transmit AP's in response to innocuous, mechanical stimuli are unlikely to form synapses with the same DH neurons. So, assuming that's the case, there probably has to be 1) some form of sensitization of the DH neurons that receive monosynaptic inputs from C-fibers or Adelta fibers (fibers that have been activated by UV exposure) and that receive polysynaptic inputs from Abeta fibers; 2) some form of sensitization of neurons, in response to ascending nociceptive transmission by spontaneously-active C-fiber inputs, that provide descending facilitatory influences, from supraspinal sites, on the release of glutamate or other mediators from Abeta-type neurons (http://scholar.google.com/scholar?q=descending+facilitation+allodynia&hl=en); or 3) some sensitization of interneurons that receive synaptic inputs from Abeta-type neurons and that themselves form synapses with the DH neurons that receive inputs from the C-fibers or Adelta fibers. Those are examples of heterosynaptic facilitation (synapses with different types of neurons in the DH producing facilitation of transmission along a common, ascending nociceptive pathway). Urban et al. (1993) probably provided the strongest evidence for central sensitization induced by UV exposure [Urban et al., 1993: (http://www.ncbi.nlm.nih.gov/pubmed/8278050)], given that those authors found that DH neurons were still spontaneously firing after the authors had performed dorsal rhizotomies, or severing of the peripheral branches of the DRG neurons innervating the irradiated skin. That independence of C-fiber inputs is fairly clear evidence of central sensitization, in my view. I think that spontaneous activity in DH neurons or changes in the excitabilities of DH neurons, evaluated in response to electrical stimulation, that are independent of the frequencies of C-fiber inputs (this would be difficult to define in the context of asynchronous C-fiber activity, but it means that the pain would be spontaneous, basically, and that the evoked, nociceptive response, in response to a mechanical stimulus, wouldn't necessarily be that much different from the steady-state nociceptive state) constitute evidence of central sensitization. UV exposure can produce spontaneous pain, although researchers usually have only reported it in older articles or case studies.
There's also a lot of research, though, showing that low-frequency C-fiber stimulation, in humans, can induce synaptic long-term depression (LTD), as opposed to long-term potentiation, of nociceptive transmission in the DH. That could account for the apparently-rapid induction of antihyperalgesic effects, following UV exposure, that last 6 hours or so [Kaur et al., 2005: (http://www.ncbi.nlm.nih.gov/pubmed/16149944); Taylor et al., 2009: (http://www.liebertonline.com/doi/abs/10.1089/acm.2008.0167)]. Some of those experimental methods that involve electrical stimulation have the potential to create confusion, because researchers sometimes use electrical stimulation to induce wind-up (as a model for and approximation of short-term central sensitization) but then use wind-up to evaluate central sensitization induced by UV exposure or another factor that induces hyperalgesia. In the case of the UV-induced augmentation of C-fiber wind-up and Abeta-fiber wind-up, the electrical stimulation that "produces" and "is" the wind-up is analogous to a sensory stimulus. The electrical stimulation of C-fibers is analogous to the heating the skin, as a way of evaluating nociceptive thresholds in C-fibers. But researchers sometimes use wind-up to induce an approximation of central sensitization and then evaluate the efficacies of, for example, antihyperalgesic drugs in relieving pain. In that case, the wind-up procedure is analogous to the UV exposure.
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