In this article [Laycock et al., 1991: (http://www.iovs.org/cgi/reprint/32/10/2741.pdf)(http://www.ncbi.nlm.nih.gov/pubmed/1654309)], Laycock et al. (1991) found that UVB exposure to only the eyes of mice latently infected with a strain of herpes simplex virus type-1 (HSV-1) reactivated the virus in the superior cervical ganglion(/ganglia) (SCG) of one mouse at four days post-UVB (Laycock et al., 1991). Some neurons whose cell bodies are in the SCG innervate the corneas of mammals [Muller et al., 2003: (http://www.ncbi.nlm.nih.gov/pubmed/12697417)], and the most that research shows clearly, in my opinion, is that UVB can either directly, through the induction of increases in the expression or release of neurotrophins or other pro-inflammatory mediators in corneal epithelial cells (corneal epithelial cells express neurotrophins), or indirectly, by the induction of changes in the firing rates of neurons in the trigeminal ganglia (TG) and caudal trigeminal nucleus (CTN), induce the neurogenic reactivation of HSV-1 in the SCG. The fact that the reactivation, in the one mouse, occurred at 4 days post-UVB might, under different circumstances (i.e. if there were more data showing the timecourse of reactivation in the SCG or in sites in the brainstem, etc.), be telling and suggest that UVB had induced the reactivation in the sympathetic ganglia by polysynaptic pathways. Loiacono et al. (2003) [Loiacono et al., 2003: (http://www.ncbi.nlm.nih.gov/pubmed/12775417)] found that UVB induced viral immediate-early gene (IEG) expression in the TG of mice. I think the idea with those experiments was to show that viral proteins are not required for reactivation of HSV by UVB, but the article also just is another one showing that UVB induces IEG expression in TG neurons and that it's not about retrograde axonal transport of viral proteins from sites of "occult" latency, or something along those lines, in corneal epithelial cells. There are some articles in which researchers purport to have shown visual-evoked potentials following UVA exposure to humans, but I think they're actually showing trigeminally-evoked potentials. There are many articles showing that visible light-induced nociceptive transmission (i.e. "photophobia") is more severe, in people who experience migraines, when nociceptive stimuli, such as thermal stimuli, are applied to the skin of the chin or nose. Neurons in the caudal trigeminal nucleus provide either monosynaptic or polysynaptic inputs to all of the sites, in the brain, at which changes, such as in IEG expression or enzyme activities, have been shown to occur, following UVA exposure to the eyes in animals. Some of those sites are the intergeniculate leaflet of the lateral geniculate nucleus (LGN) of the thalamus, the ventral LGN (vLGN), the superior colliculus, the visual cortex, and the nucleus of the optic tract [Amir and Robinson, 1995 and 1996: (http://scholar.google.com/scholar?hl=en&q=Amir+Robinson+ultraviolet)]. Neurons in the vLGN provide inputs to the SCN, etc.
In rats and mice and, to a lesser but significant extent, humans, the anatomy of the nasociliary subdivision of the ophthalmic branch of the trigeminal nerve and of the ciliary ganglia, which the nasociliary nerve fibers carrying afferent action potentials to the CTN extend through and do not form synapses within, means that the optic nerve transection procedures, used in some of the articles, could have severed fibers of the nasociliary nerve or the ciliary nerve (which the nasociliary nerve fibers fuse with, at different sites, in different species, along the surfaces of the optic nerve). In some species of mice, there are five ciliary ganglia (CG) (some of which are referred to as accessory ciliary ganglia) on different faces of each optic nerve and oculomotor nerve, and the distribution of the CG fibers that extend along the surface of each optic nerve, posterior to the eye (the "globe"), would make it almost impossible to transect or crush the optic nerve without damaging the CG nerve fibers.
It's worth noting that it wouldn't be ethical or possible to expose human eyes to artificial UV sources, because the eyes normally absorb mostly diffuse UVB and UVA. The UV is absorbed by gas molecules in the atmosphere and scattered in all directions, and the cornea and lens absorb diffuse UV from all directions. The epithelial cells in the corneas are much more densely innervated than the epithelial cells in the skin (keratinocytes) are, and that's one reason it wouldn't be possible to use direct ocular UVB or UVA in research on humans. The research on photokeratitis or sunlight-induced keratoconjunctivitis, etc., just shows that the eyes are not equipped to handle much direct UV (http://scholar.google.com/scholar?hl=en&q=photokeratitis). It's not entirely clear why it's the case. I think one reason might be that there are more free nerve endings (and not just a higher density of nerve endings per se) in the corneas than in most skin sites. Someone could do fMRI research, like this [Moulton et al., 2007: (http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=2034350&blobtype=pdf)(http://www.ncbi.nlm.nih.gov/pubmed/17407825)], showing UVB-induced augmentation of third-order neuronal nociceptive pathways, but people would probably still say that the effects could have resulted from a peripheral component to the allodynia or thermal hyperalgesia. One could almost always say that, and there seem to be some researchers who want to think of the central nervous system as being "inviolable." I'm exaggerating, but there honestly does seem to be resistance to the idea of central sensitization, in general. There's actually an interesting article in which the researchers argued that they had shown UV "vision" or discrimination in rodents, but I think it could have been that the rodents were experiencing UV-induced increases in the frequencies of action potentials in CTN neurons (via increases in the firing rates of TG neurons), imposed upon a lower-frequency, asynchronous firing pattern of those neurons. I mean that there could be a difference in the firing pattern *during* UV exposure, as opposed to the firing pattern 30 or 60 or whatever minutes after exposure. As far as I know, no one has measured the firing patterns of single C-fibers or Adelta fibers during UV exposure, but those types of trigeminally-evoked potentials in the occipital cortex could be showing that type of effect. The neurons in the TG and CTN could display a more synchronous firing pattern during UV (or a higher-frequency firing pattern that is as asynchronous as the pattern found during the background, post-exposure period of time), but that may not be the case.
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