This article [Burstein and Jakubowski, 2009: (http://www.springerlink.com/index/W31254628P581268.pdf)] looks like one that might provide a good discussion of the anatomical pathways by which changes in the firing rates/patterns of (or changes in the axonal transport of neurotrophins within, etc.) neurons in the trigeminal nucleus caudalis (TNC) (caudal trigeminal nucleus, etc.) could influence something like seasonal affective disorder. This article [Bolay et al., 2002: (http://www.nmr.mgh.harvard.edu/DOT/PDF/nm_csd.pdf)(http://www.ncbi.nlm.nih.gov/pubmed/11821897)] is a good one that describes some of the mechanisms underlying trigeminovascular reflexes in migraines, but all or most of the mechanisms are relevant to future research on the effects of ultraviolet radiation (UVR) on the brain. Two mechanisms by which UVR exposure could influence cerebral blood flow would be through the induction of efferent action potentials, originating in the TNC, in trigeminal ganglion (TG) neurons whose peripheral terminals are in the meningeal arteries or the pial arterioles (Bolay et al., 2002) or through an increase in the firing rates of preganglionic parasympathetic neurons in the superior salivatory nucleus (SSN) and, as a result, of parasympathetic neurons in each of the sphenopalatine ganglia (SPG) (a.k.a. pterygopalatine ganglia) that provide efferent inputs to the meningeal and pial arteries. The release of vasoactive intestinal peptide, nitric oxide, and acetylcholine from [Hamel, 2006: (http://jap.physiology.org/cgi/reprint/100/3/1059)(http://www.ncbi.nlm.nih.gov/pubmed/16467392?dopt=Abstract)] from the perivascular terminals of those SPG neurons is then thought to induce afferent action potentials in TG neurons, originating at the peripheral terminals of those TG neurons, that produce feed-forward activation of neurons in the TNC, etc. Neurons in the TNC are thought to not project directly to preganglionic neurons in the SSN but to, conceivably, provide monosynaptic inputs to neurons in the parabrachial nucleus and thereby activate neurons in the SSN via polysynaptic pathways. This is not all that relevant to the issues at hand, but that's a fairly well-established pathway and is interesting to know about in a superficial way. Neurons in the TNC provide efferent inputs to sites all over the brain, though. There are some articles showing that UVB increases subcutaneous blood flow, and that effect is likely to result from changes in the firing rates of neurons in the spinal cord or brainstem. Some of those effects might be sensory-autonomic "reflex-like" effects (or, in the case of facial UVR exposure, trigeminovascular autonomic response) or might be just dorsal root reflexes or another process that just depends on the existence of two or more primary afferent neurons (one transmitting an afferent action potential, from the UV-irradiated skin to the dorsal horn, and the other transmitting an efferent action potential to the subcutaneous blood vessels). But the authors [Petersen and Kristensen, 1990: (http://www.ncbi.nlm.nih.gov/pubmed/1980982)] make a compelling argument that the effect couldn't be due to the diffusion of vasoactive mediators from the dermis to the subcutaneous tissue, given that the blood supplies to the cutaneous and subcutaneous tissues are independent of each other. In a reply to a correspondence about their article, the authors also fairly convincingly ruled out some sort of diffusion effect in the lymphatic fluid.
The other thing that's interesting is the discussion, in this article [Streilein et al., 1999: (http://www.ncbi.nlm.nih.gov/pubmed/10816653)], of the reasons for the "substance P" tolerance/tachyphylaxis effect that tends to occur in response to UVR exposure. The authors basically found that substance P enhances contact hypersensitivity (CHS) responses initiated in the skin, and UVB reliably suppresses the initiation phase (and elicitation phase) of CHS responses. Thus, because of that and other lines of evidence, the authors made the argument that UVB seems to preferentially increase the effects of CGRP over those of substance P. The authors suggested that one reason for the effect may be that substance P is much more rapidly degraded by aminopeptidase enzymes and other neuropeptide-degrading enzymes than CGRP is [these are some articles discussing that, and some have been cited in the articles by Streilein and colleagues: (http://scholar.google.com/scholar?hl=en&q=Matsas+1984+aminopeptidases)].
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