Fundamental Discoveries in Biology: Gillardon and Colleagues

I'm not sure if this is the first or one of the first articles to show spontaneous action potentials following UVB [Gillardon et al., 1992: (http://www.ncbi.nlm.nih.gov/pubmed/1637107)] (it's definitely one of those first series of papers showing the mechanisms). (I don't have it in electronic format but only have it in photocopied form, and I haven't downloaded it yet, since the electronic journals became available going back decades.) That paper and the related paper(s) that show, when viewed together, that CGRP was evidently being released in the spinal cord, following UVB and in response to the asynchronous firings of C- and Adelta-fibers, are a huge discovery in science in the 20th century, in my opinion. They lead to a cascade of implications that just shouldn't be ignored, in my opinion. It's a fundamental discovery in biology, just as the research on the effects of visible light was fundamental and profound. It's possible that those sensory mechanisms don't regulate brain function via changes in the firing rates of, or axonal transport in, etc., neurons in the caudal trigeminal nucleus, but I'd be very surprised if that turns out to be the case. In any case, I've certainly never made any scientific discoveries, and it's very unlikely that I'll be making any scientific discoveries in the future. That old paper of mine wasn't much more than a cataloguing of mechanisms, along with some interpretations thrown in. I think this is that article I was thinking of [Streilein et al., 2000: (http://www.ncbi.nlm.nih.gov/pubmed/11268357)] that discusses the fact that the release of neuropeptides into the aqueous humor, from sensory fibers and other classes of neurons, contributes to anterior chamber-associated immune deviation ("immune privilege"). I couldn't discuss this in that paper, because it would have meant complicating matters even more, but it's similar to the research showing that CGRP released into the skin, through dorsal root or axon reflexes, in response to UVB exposure, produces interleukin-10-dependent immunosuppressive effects, etc. But that's the type of mechanism that could be a source of confusion in research, because the C-fibers innervating the side of the face, say, could fire asynchronously and, after causing interneurons to fire, induce efferent action potentials in other C-fibers and induce neuropeptide release (substance P, vasoactive intestinal peptide, CGRP, alpha-MSH, etc.) in the iris and ciliary body. Here's another paper that discusses the role of visible light in regulating ACAID [Ferguson et al., 1995: (http://www.jimmunol.org/cgi/content/abstract/155/4/1746)]. Alpha-MSH is a primitive neuropeptide, incidentally. It can have really strong anti-inflammatory effects, and I don't quite understand what the reasons for that are. It decreases NFkappaB activation in the cytosol and thereby limits the interleukin-1beta-induced increases in pro-inflammatory cytokine expression, but I don't quite understand why that would account for its supposed potency. A lot of things decrease NFkB activation.

In any case, it's interesting, and, when one steps back and looks at the research itself, by Gillardon and colleagues (I think they did most of them), the papers are amazing to me. They're very short, in general, and very simple experiments. But they have pretty profound implications for mammalian biology, in my opinion, and, arguably, for thermoregulation in both mammals and in lower organisms. It's strange that some huge discovery like that, by Gillardon and colleagues, could go unrecognized, and it shouldn't be the case.