Neurons in the Caudal Trigeminal Nucleus That Provide Monosynaptic Inputs to the Hypothalamus (And Receive Monosynaptic Inputs From the Facial Skin)

This article [Matharu, 2007: (http://www3.interscience.wiley.com/journal/120795529/abstract)] is great, and the authors discuss research showing changes in hypothalamic metabolite ratios, measured using magnetic resonance spectroscopy, in association with migraines or with cluster headache. Especially if one doesn't try to put too much emphasis on the specific changes associated with each condition (this is the approach the authors have taken), the article is great. The discussion on p. 966 (p. 4 of the pdf) about the direct inputs from to the hypothalamus [the authors cite reference 24, which is Malick and Burstein, 1998: (http://www.ncbi.nlm.nih.gov/pubmed/9762871)] from the caudal trigeminal nucleus (the trigeminal subnucleus caudalis is, as far as I remember, the caudal trigeminal nucleus, which I think is also called the "spinal nucleus of V" and the "trigeminal sensory nucleus" and the "trigeminal nucleus caudalis," etc.). That article by Malick and Burstein (1998) looks fantastic. The abstract discusses neurons with cell bodies in the caudal trigeminal nucleus that, based on retrograde labeling from parts of the hypothalamus, receive monosynaptic inputs from the central terminals of trigeminal ganglion neurons innervating the corneas, skin, etc. I'll try to make sense of it, but I think part of the reason for the strange sensory triggers for migraines is, as Malick and Burstein (1998) intimate in that abstract, that the afferent inputs, to the caudal trigeminal nucleus, from the cerebral blood vessels and the afferent "inputs" from the skin of the face are somewhat convergent and converge on even the same neurons in the caudal trigeminal nucleus. So when a person has a migraine from sitting in the sun or from heat, there can be poorly-regulated efferent activity induced in the trigeminal ganglion neurons innervating the meningeal arteries, etc. (http://scholar.google.com/scholar?hl=en&q=activity+meningeal+afferent+efferent+trigger+migraine). I'm not suggesting that that's, by any means, a mechanistic statement or the only "mechanism," but it's interesting.

Here are some interesting articles that look like they discuss some trigeminal pathways in snakes (snakes that have infrared receptors), presumably meaning sensory neurons that are activated in response to radiation in the infrared wavelengths and that produce secondary changes in the firing rates of neurons in the trigeminal sensory nucleus/nuclei of snakes. Maybe that's involved in autonomic thermoregulation in some organisms or something. I don't know, but it's interesting to consider. Some of those articles look interesting (http://scholar.google.com/scholar?hl=en&q=%22autonomic+thermoregulation%22+trigeminal). Some of them talk about "fever," and it's almost like the effects of UVB are like a "controlled fever" or "fever-by-proxy." Subjectively speaking, it's almost like some kind of primitive, induced fever that's driven, initially, by increases in neuropeptidergic and glutamatergic transmission and, possibly, pro-inflammatory cytokine expression in astrocytes in the hypothalamus, etc., in response to UVB (http://scholar.google.com/scholar?hl=en&q=trigeminal+thermoregulation+sensory+hypothalamus). Then there may be some adaptation or response, to downregulate those effects, that may or may not occur readily. In any case, these are fairly unscientific statements, but it's an interesting area to think about.