This article [Arbab et al., 1992: (http://www.ncbi.nlm.nih.gov/pubmed/1481736)] describes the anatomical pathways that could allow ultraviolet B (some of the articles describing the use of "UVA" to induce sunburn pain are likely to be really showing effects mainly mediated by UVB; if even 1 percent of the irradiance of a source of UV radiation is in the UVB wavelengths, this small amount of UVB can be responsible for something like 95 percent of the biological effects) to influence cerebral blood flow or the degranulation of perivascular mast cells, etc. (this is in reference to a paper of mine that I posted a couple of days ago). The authors cite research showing that severing the peripheral branches of some trigeminal ganglion nerve fibers of the maxillary and ophthalmic divisions of the trigeminal nerve can reduce the diameter of the ipsilateral cerebral arteries by 25 percent, meaning that CGRP and substance P and other mediators are released, in response to efferent action potentials that are probably originating in the caudal trigeminal nucleus, from the peripheral terminals of trigeminal ganglion neurons and contribute, under baseline conditions, to the dilation of the middle cerebral artery, etc. There's also quite a bit of research on the role of neuropeptides released from C-type trigeminal ganglion neurons (the nomenclature is slightly different for different classes of trigeminal ganglion neurons, but they can still be called C-fibers, etc.) and the trigeminal nucleus in vasospasm, following subarachnoid hemorrhage (http://scholar.google.com/scholar?q=trigeminal+vasospasm+subarachnoid&hl=en&lr=). And electrical stimulation of the trigeminal ganglion can influence cerebral blood flow (http://scholar.google.com/scholar?num=100&hl=en&lr=&q=%22cerebral+blood+flow%22+trigeminal+ganglia+OR+ganglion). There are different types of trigeminal root reflexes, and they're not the same as dorsal root reflexes. But the underlying concept is similar. The concept is that two trigeminal ganglion neurons are required. An afferent action potential in a trigeminal ganglion neuron, originating from the skin of the face or the corneal epithelial cells on the surface of the eye, which is innervated by trigeminal ganglion neurons of the ophthalmic branch of the trigeminal nerve, travels to the caudal trigeminal nucleus and activates an interneuron, for example. GABA or glutamate released from the interneuron depolarizes the central terminal of a second trigeminal ganglion neuron (part of the reason this could occur relates to the anatomical relationships between some interneurons and the central branches of trigeminal ganglion neurons whose peripheral branches terminate at a wide variety of locations) and produces an efferent action potential. This can induce CGRP or substance P release at sites adjacent to the middle cerebral artery, etc., thereby causing headaches or just vasodilation or thromboses or remodeling of the smooth muscle cells, because of the release of mast cell proteases by degranulating mast cells, or any number of other effects. Dorsal root reflexes have been suggested to be a mechanism whereby sensory inputs can be "refined," so that more efferent action potentials are being induced or suppressed in some C-fibers in response to specific nociceptive or inflammatory activity in some location that is innervated by other C-fibers or Adelta fibers, etc. A similar type of "refining" effect could occur in the trigeminal nucleus, but the result could also be just inflammatory hyperalgesia and ongoing damage and inflammation, etc.
These mechanisms could, therefore, easily produce or account for pathological changes in the cerebral blood vessels, and much of this research has been done in the context of migraines and other pathological disease states that involve the trigeminal system. But basic research has become devalued to an absurd extent in some of these areas, and it seems as if these types of mechanisms are of no interest whatsoever to anyone. Of course, if one buys into some of the dogma, there is no regulation of cerebral blood flow by neuronal activity. That's obviously not true, in my opinion, although the extent to which neuronal regulation ("nervous regulation") influences cerebral blood flow is likely to be less in a person who is in perfect health than in a person who is not. And UV exposure would obviously be more likely to produce pathological effects in a person in a disease state, in my opinion, than in a person who is not in a disease state. But my main point is just that all of the crazed dogma, in some of these areas, can ultimately confound all attempts to view biological processes in an objective and "scientifically-curious" manner. There's a disturbing kind of arrogance in trying to put a value-laden spin on some of these fundamental processes in biology.
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