My old paper is such a God-awful, rambling thing (http://hardcorephysiologyfun.blogspot.com/2009/05/another-old-paper-of-mine.html), that I thought I should attempt to summarize some of the mechanisms I reviewed in it. The overall concept is that UVB causes these "early mediators," such as prostaglandins and bradykinin, to be rapidly induced, within minutes of exposure. Some of these early responses are just mediated by superoxide production or by the activation of phospholipase enzymes, etc. These early-phase mediators, which cis-urocanic acid is also an example of, act on sensory nerve fibers innervating the epidermis and either directly induce axon reflex-mediated vasodilation or sensitize C-fibers and Adelta-fibers [the dorsal root ganglion (DRG) neurons] to the more potent actions of UVB-induced nerve growth factor and interleukin-6 and TNF-alpha, all of which are expressed in UVB-irradiated keratinocytes and cause the stronger, sustained effect of inducing "spontaneous" (but obviously not spontaneous) action potentials by acting directly on the peripheral terminals of DRG neurons innervating the epidermis. An axon reflex occurs when an action potential only travels to a branch point in a C-fiber, with the second "branch terminal" or arborization innervating the dermis and terminating at a blood vessel. The action potential "becomes" efferent at the branch point and then travels to the "second terminal" of the peripheral branch of the C-fiber, in the skin. Some of these apparent axon reflexes may, in fact, be dorsal root reflexes, however. There can also be weaker currents in C-fiber terminals that are not actual action potentials but that could cause neuropeptide release. But then, once DRG neurons begin to fire en masse, asynchronously, the action potentials traveling to the dorsal horn or, in response to UVB-irradiated facial skin, the caudal trigeminal nucleus and release CGRP and substance P and glutamate from their central terminals into the dorsal horn or caudal trigeminal nucleus. The CGRP and substance P then act on interneurons or spinothalamic tract neurons or spinoreticular tract or "trigeminothalamic tract" neurons, etc. As a result, the firing of these neurons can induce neurotransmitter release at segments rostral to the spinal segments at which the C-fibers releasing them entered the dorsal horn, and this type of polysynaptic transmission has been shown to occur in the spinal cord in response to UVB exposure of the skin.
It has also been shown in response to UVB exposure of the eyes of rodents, but the anatomical pathways are obscure. The action potentials probably just go to the trigeminal nucleus, from the trigeminal ganglion neurons innervating the corneas, and then cause neurons projecting from the caudal trigeminal nucleus to the hypothalamus to fire and cause hypothalamic neurons to induce the release of alpha-MSH from the pituitary, etc. (the effect could be blocked by hypophysectomy or ciliary ganglionectomy). I'm saying that because the ciliary ganglionectomy procedure may have actually cut some trigeminal ganglion nerve fibers passing through the accessory ciliary ganglion, I think it's called. I looked into the anatomical possibilities in detail but was nonetheless not able to definitively narrow down the possibilities. The anatomy is surprisingly complex, and I think the peripheral branches (sometimes referred to as "postganglionic" fibers, even though they're sensory neurons) of some trigeminal ganglion neurons travel through the ciliary ganglia and on to the caudal trigeminal nucleus. I forget the details, but it's another example of polysynaptic neurotransmission induced in response to UVB exposure to the skin. I explained the way dorsal root reflexes work in a previous posting, and it's noteworthy that GABA produces depolarization, not hyperpolarization, of the central terminals of C-fibers and Adelta fibers, upon its release from interneurons in response to other C-fiber inputs [a dorsal root reflex requires two separate C-fibers (C-type DRG neuron) or one C-fiber and an Adelta fiber, etc., and the feature that distinguishes it from an axon reflex is that the efferent action potential begins in the dorsal horn, at the central terminal of the "second" C-fiber in response to GABA receptor activation on the C-fiber].
There are obviously many other parts of the brain that would be likely to be affected, but there hasn't been much research, since the 1990s, on the changes that occur in the spinal cord. To my knowledge, no one has examined the specific phenotypic changes that would be expected to occur in the trigeminal nucleus or other parts of the midbrain or brainstem, for example, in rats exposed to UVB. Presumably, someone is interested in doing basic research in photobiology/photoneuroimmunology and learning what the effects on the circadian rhythm are. It's very likely that there are effects on circadian neurobiology, etc., and that they occur via the sensory nerve fibers.
The general idea behind systemic immunosuppression induced by UVB is that Langerhans cells, which are immature dendritic cells in the skin, are induced to migrate to regional lymph nodes in large numbers, within 6 hours or so of UVB exposure. They can induce tolerance to skin-associated or skin-derived antigens because they never mature, essentially. I'm forgetting why their migration precludes their maturation, but immature dendritic cells are tolerogenic. The infiltration of monocytes and neutrophils into the skin, at various time points after exposure, is also required for UVB-induced systemic suppression of delayed-type hypersensitivity to protein antigens injected intradermally into the UVB-exposed site, right after exposure. Different types of cells are constantly infiltrating into and migrating from the skin in response to UVB exposure, and these cells are acted upon by cytokines released from mast cells in the skin and from keratinocytes, etc. The infiltrating monocytes and neutrophils also release cytokines that act on keratinocytes and sensory nerve fibers, etc.
These are not just effects that result from increases in skin temperature or from some other nonspecific effect, because the researchers controlled for that by using cold UV sources and controlling for skin temperature and also because the phenotypic changes in the spinal cord can last up to 7-9 days. It'll probably be another 20 years before anyone does the research, though, the way things are now. It's unfortunate, because it's an interesting set of mechanisms. Obviously, these are potentially very damaging effects, and I would strongly urge anyone to talk with his or her doctor, very seriously, before receiving any sun exposure.
I'm explaining this because it's interesting and because researchers have been bullied, over the years, into not discussing it or even looking at the research, seemingly. The research has been sitting around for almost 20 years, while all the (anti-)intellectual bullying has gone on and led nowhere.
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