The author of this article [Berkley, 2005: (http://www.ncbi.nlm.nih.gov/pubmed/16139851)] wrote this in the abstract (I'm going to look at the full text now):
"Throughout the CNS, neurons responsive to stimulation of the reproductive tract also respond to stimulation of skin and other internal organs, in a manner modifiable by reproductive status and peripheral pathophysiology."
I'm wondering if cutaneous UVB exposure (the exposure might very well not have to be on sites innervated by C-fibers whose central terminals are in the L1 and T13 dorsal horn) might affect placental blood flow (by producing primary afferent depolarization and inducing efferent action potentials in visceral primary afferent neurons) via changes in the activities of neurons, originating in the spinal cord at sites rostral to the L1 and T13 dorsal horn or at supraspinal sites, that exert a descending influence on the central terminals of visceral primary afferent neurons (T13 and L1 dorsal root ganglion neurons). I'm not, in any way, suggesting that anyone go in the sun without talking to one's doctor, and I'm just discussing my more extreme thoughts on these topics. This may well not be true, but I'm just saying it seems like it might be possible. Berkley (2005) discusses some of the evidence that visceral and somatic (such as cutaneous) primary afferent neurons converge on the same neurons in the dorsal horn [or maybe converge, via intervening interneurons or other neurons, on tertiary sites (i.e. neurons) in the dorsal horn (http://scholar.google.com/scholar?hl=en&q=tertiary+convergent+neurons+dorsal+horn)].
This article [Amira et al., 1995: (http://ep.physoc.org/content/80/4/645.full.pdf)(http://www.ncbi.nlm.nih.gov/pubmed/7576603)] is not all that good an example of anything, and I was looking at it before I found that article by Berkley (2005). But the article by Amira et al. (1995) discusses some of the growth of and changes in the sensory innervation of uterine structures during pregnancy in rats.
Researchers have suggested that CGRP may be involved in the regulation of placental blood flow (http://scholar.google.com/scholar?hl=en&q=CGRP+placental+blood+flow), and an increase in the release of CGRP from DRG neurons innervating the placenta might both increase or otherwise regulate (potentially producing adverse effects, although I'm not attempting to make any values-based or subjective statements in this posting) placental blood flow [I think Mowa and Papka, 2004, listed in this search result, appear to have discussed the capacities of visceral primary afferent neurons to conduct efferent action potentials and exert "efferent effects" on their visceral target tissues, as primary afferent neurons are known to do (discussed in past postings of mine): (http://scholar.google.com/scholar?hl=en&q=efferent+primary+afferent+CGRP+placenta)]. Dong et al. (2003) [Dong et al., 2003: (http://molehr.oxfordjournals.org/cgi/content/full/9/8/481)(http://www.ncbi.nlm.nih.gov/pubmed/12837925?dopt=Abstract)] discussed the fact that CGRP had been found to reduce placental vascular resistance (i.e. produce vasodilation) in in vitro experiments and that CGRP is a very potent vasodilator. They discuss the fact that plasma CGRP levels even increase during pregnancy. UVB-mediated increases in CGRP release in the placenta could regulate the IgG subclasses (i.e. IgG1, IgG2, and IgG3 isotypes, etc.) that cross the placenta [with reference to the issue of the fetus as constituting, for all practical purposes, an "allograft," as discussed by Niederkorn and Wang (2005) (discussed below)] [Niederkorn and Wang, 2005: (http://www.ncbi.nlm.nih.gov/pubmed/16314777)] or even regulate Th1/Th2 immunological development in the fetus. I'm just suggesting these possibilities and am not suggesting anything beyond that. I link to a search (http://scholar.google.com/scholar?hl=en&q=CGRP+placenta+immune) on the potential role of CGRP in fetal immune privilege (or placenta-associated immune privilege or whatever one wants to call it, given the variety of terms used to describe it) below [or, actually, these searches are better: (http://scholar.google.com/scholar?hl=en&q=fetal+%22immune+privilege%22); (http://scholar.google.com/scholar?hl=en&q=fetal+%22immune+privilege%22+CGRP)]. On the other hand, there's a reference in that search (Parida et al., 1996) suggesting that elevations in CGRP might produce adverse effects. But Parida et al. (1996) (http://journals.lww.com/pedresearch/pages/articleviewer.aspx?year=1996&issue=04001&article=00399&type=fulltext) looked at cord blood concentrations of CGRP, and elevations in blood CGRP are not likely to be produced by the same factors or conditions that may produce localized increases in CGRP release in the placenta (i.e. UVB). For example, Parida et al. (1996) note that elevations in CGRP can occur during sepsis. That's obviously a very different set of circumstances than anything I've been talking about, and one can't conclude much, in my opinion, about localized changes in peptidergic transmission by looking at changes in blood levels of CGRP or other neuropeptides. But there is the potential for some sort of deficiency in the normal adaptations that might be expected to occur (the adaptive changes in axonal transport or refinement of sensory transmission associated with the occurrence of "more" dorsal root reflexes) in response to the supposed UVB-mediated increases in spontaneous, efferent activities of primary afferent neurons innervating the placenta. In any case, CGRP could conceivably fulfill a "similar" role to that of estriol, a hormone that increases during pregnancy. Estriol has been researched in the treatment of multiple sclerosis (http://scholar.google.com/scholar?hl=en&q=estriol+%22multiple+sclerosis%22+pregnancy), because autoimmune or inflammatory symptoms can sometimes become less severe during pregnancy (potentially in an estriol-dependent manner). Those chang
The article by Niederkorn and Wang (2005), in this search result (http://scholar.google.com/scholar?hl=en&q=CGRP+placenta+immune), makes comparisons between ocular (eye-associated) immune privilege [anterior chamber-associated immune deviation (ACAID)]. I'm assuming they discuss CGRP to a significant extent, because ACAID is known to be dependent on CGRP, as discussed in past postings. In any case, these mechanisms might be relevant to the etiologies of disease states that have been associated with low levels of UVB exposure (multiple sclerosis and schizophrenia) [(http://scholar.google.com/scholar?hl=en&q=UVB+schizophrenia); (http://scholar.google.com/scholar?hl=en&q=UVB+%22multiple+sclerosis%22); (http://scholar.google.com/scholar?hl=en&q=CGRP+%22multiple+sclerosis%22)]. As discussed in past postings, vitamin D analogs have been shown to upregulate CGRP mRNA in dorsal root ganglion neurons, in an NGF-dependent manner [Riaz et al., 1999: (http://scholar.google.com/scholar?hl=en&q=CGRP+%22vitamin+D%22+dorsal+root)]. Vitamin D deficiency has also been linked to the development of peripheral neuropathy, in some cases [it looks like Carlson and Kenny, 2007, may have discussed that possibility: (http://scholar.google.com/scholar?cites=4360282027492426919&hl=en)].
That's not a good thing to see, in my view. I didn't realize there was that research on maternal-fetal immune privilege. Hopefully these suggestions aren't valid, but, when I decided to explore that potential mechanism that flowed out of the UVB research by Gillardon and colleagues and by other researchers, I didn't know there was all of that research (on the actions of CGRP, outside of the context of UVB, at the maternal-fetal interface). I guess there's maybe not a massive amount of research, but yeah...
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