(I should mention, again, that direct UV exposure to the eyes would be expected to damage the trigeminal nerve terminals in the corneas and could, conceivably, produce outright damage to parts of the brain. Most UVB and UVA that reaches the eyes is diffuse, as opposed to direct, UVB/UVA (Sliney, 1997, cited below), and direct UV exposure to the corneas does not occur, to a large extent, under normal, everyday circumstances or even when a person is looking at choppy water or snow or other "surfaces" that reflect large percentages of the direct UV radiation that they absorb.)
In this article [Sliney, 1997: (http://cat.inist.fr/?aModele=afficheN&cpsidt=2855724)], Sliney (1997) discusses the fact that the apparent transmittance of radiation at UVA wavelengths (315 or 320 to 400 nm) by the lens can be spuriously elevated because of fluorescence in the lens. Tryptophan and other fluorophores in the lens can absorb (and undergo excitation in response to the absorption of) radiation at UVA wavelengths and then emit radiation at visible wavelengths or at other, longer wavelengths within the UVA spectrum [Van den Berg, 1993: (http://www.iovs.org/cgi/reprint/34/13/3566.pdf)(http://www.ncbi.nlm.nih.gov/pubmed/8258514)], and that phenomenon could partially account for some of the evoked potentials, measured by electrodes on the occipital scalp in humans, that researchers have found in response to very brief pulses of high-intensity, direct UVA radiation directed at human eyes [Brainard et al., 1999: (http://www.ncbi.nlm.nih.gov/pubmed/10363758)]. I tend to think that those are primarily trigeminal(ly) evoked potentials, however, given the longer latencies and the fact that UV may induce spontaneous activity in mechanosensitive trigeminal afferent neurons. That spontaneous activity in Adelta fibers, for example, and sensitization, via UV-induced changes in the firing patterns of neurons in the trigeminal nucleus caudalis (TNC), of neurons in the superior colliculus (or other sites that receive inputs from both TNC neurons and retinal neurons) could produce the evoked potentials in the visual cortex. The retinas could have been exposed to a low-level, "background" irradiance of visible light, as a result of the emission of visible light from UVA-excited fluorophores in the lens, and the evoked potentials in the occipital cortex could have resulted from the combination of those low-level, visual stimuli with the UVA-induced sensitization of TNC neurons and nociceptive transmission along "multisensory" pathways from the superior colliculus, etc., to the visual cortex. There could also have been a minor contribution of attentional or cognitive, stress-related influences on visual-evoked potentials. But the point is that sensitization of TNC neurons can occur very rapidly, in response to trigeminal stimulation, and it's unlikely that any meaningful amounts of UVA were transmitted to the retinas and acted on the retinas directly. It's also possible that the high-intensity pulses of UVA directly activated trigeminal nerve fibers by atypical mechanisms, such as those by which lasers can evoke action potentials in single C-fibers, etc.
There's also research in which researchers have used electroretinograms or even spiral-cuff electrodes (or similar devices, supposedly used to measure transmission along the optic nerves) to measure action potentials that were supposedly being transmitted along the axons of retinal neurons in the optic nerves, but those devices could have also been measuring action potentials in the axons of ciliary ganglion neurons or in the axons of trigeminal ganglion neurons that innervate the corneas and that are contained within the ciliary nerves, which themselves extend along sections of the surfaces of the optic nerves in rats, mice, and humans. Summation of subthreshold potentials can occur in the dendrites (and potentially the axon terminals) of some ciliary ganglion neurons in rabbits, for example, and those "subthreshold neurons" have multiple synaptic inputs [Johnson and Purves, 1983: (http://jp.physoc.org/cgi/reprint/339/1/599.pdf)(http://www.ncbi.nlm.nih.gov/pubmed/6887037)]. That feature distinguishes the subthreshold ciliary ganglion neurons from the suprathreshold ciliary ganglion neurons that can only fire in response to suprathreshold excitation by their single-neuron inputs from preganglionic, ChAT+ parasympathetic neurons in the Edinger-Westphal and anteromedian nuclei. Some ciliary ganglion neurons innervate the corneas, and it's conceivable that UVA could induce antidromic action potentials to develop in corneal or iridial terminals of ciliary ganglion neurons. But the measured action potentials seem most likely to have been propagating along the axons of trigeminal ganglion neurons in the ciliary nerves, etc. Another issue that hasn't been addressed adequately is the role that UVA- or UVB-induced neurotrophin expression and release, by corneal epithelial cells or keratinocytes in the skin, may have in producing phenotypic changes in neurons that innervate the corneas or irises and whose cell bodies are in the ciliary ganglia, superior cervical ganglia, or trigeminal ganglia. It's conceivable to me that the axonal transport of neurotrophins, from the skin to the cell bodies of those neurons (or to the TNC, from the corneal terminals of trigeminal ganglion neurons, for example), could be increased substantially in response to UVB or UVA exposure, but those effects obviously wouldn't emerge immediately. But there's also plenty of research, incidentally, showing that the release or expression of brain-derived neurotrophic factor (BDNF) by primary afferent neurons can be increased in response to the application of inflammatory stimuli at the peripheral terminals of those primary afferent neurons (http://scholar.google.com/scholar?hl=en&q=skin+%22C-fiber%22+BDNF+%22dorsal+horn%22+OR+trigeminal), and it's possible that the UV-induced spontaneous activity in dorsal horn or TNC neurons (resulting from UV-induced changes in neurotrophin trafficking or intracellular signalling cascades or action potentials in primary afferent neurons) could cause BDNF to be released in different parts of the brain. UV exposure could induce "activity-dependent" changes in BDNF signalling in the brain that could partially mediate the supposed influences of UVB and UVA on seasonal affective disorder, etc. (http://scholar.google.com/scholar?hl=en&q=activity-dependent+BDNF+%22dorsal+horn%22+OR+trigeminal). I just mean that changes in CGRP and substance P release, in different parts of the brain, wouldn't have to be the only mechanisms.
I've also seen articles, outside of the context of UV research, in which researchers have used the same types of electrodes to measure action potentials, transmitted along the ciliary nerves that extend along the surfaces of the optic nerves, induced by sensory transmission from the corneas as other researchers have used to measure action potentials induced by retinal illumination. In one case, researchers assume that the action potentials are being carried along the axons of trigeminal ganglion neurons, and, in the other case, researchers assume that the action potentials are propagating along the axons of retinal neurons. But those assumptions cease to be useful when the sites at which the action potentials are originating are unknown, as in the context of UVA exposure to the corneas.
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