Corneal or Facial UVA Regulates Pineal Serotonin N-Acetyltransferase Activity and Induces IEG Expression in Suprachiasmatic Nucleus and Thalamus, etc.

These articles [including Amir and Robinson, 1995: (http://scholar.google.com/scholar?cites=16094207976236452086&hl=en); Zawilska et al., 2000: (http://www.springerlink.com/content/h85730283542l8w3)] show that cutaneous and corneal exposures to ultraviolet A wavelengths can induce immediate-early gene expression in parts of the thalamus, most parts of the suprachiasmatic nucleus (SCN), and other parts of the hypothalamus adjacent to the SCN. Some of those articles also show that UVA wavelengths (some of the authors refer to UVA wavelengths as being near-ultraviolet wavelengths) regulate serotonin N-acetyltransferase activity in a manner that's sensitive to inhibition by adrenoreceptor or glutamate receptor antagonists, etc.

The authors attribute the effects to UVR-induced actions in the retinas, but all or most of those effects could be explained in terms of UVR-induced increase in the firing rates of neurons in the trigeminal ganglion and, consequently, caudal trigeminal nucleus (CTN). The noradrenergic regulation of pineal serotonin N-acetyltransferase activity (Zawilska et al., 2000) could be explained in terms of the projections of CTN neurons to adrenergic cell groups in the brainstem that innervate the pineal gland or could be due to the innervation of the superior cervical ganglia (SCG) by trigeminal ganglion or CTN neurons [because the SCG or the axons that pass through them, without forming synapses, are required for the normal maintenance of the pineal melatonin rhythm (http://scholar.google.com/scholar?hl=en&scoring=r&q=%22pineal+gland%22+%22superior+cervical+ganglia%22&as_ylo=2004)], etc. Also, neurons in lamina I of the CTN and in deeper laminae of the DH project to the SCN or accumulate tracers after retrograde axonal transport of the tracers from the SCN [Krout et al., 2002: (http://www.ncbi.nlm.nih.gov/pubmed/11882374)], and Krout et al. (2002) discussed the fact that nociceptive transmission can regulate circadian rhythms. I'm fairly sure that the finding by Amir and Robinson (1995) that optic nerve transection can block the effects could be explained in terms of damage, induced unintentionally, to the nasociliary nerves, which are subdivisions of the ophthalmic division of each trigeminal nerve and contain the peripheral branches of the axons of trigeminal ganglion neurons that innervate the corneas, or to the axons of ciliary ganglion neurons. The axons of ciliary ganglion neurons project to the eyes along the surfaces, or external surfaces, of the optic nerves/optic nerve sheaths, to a particularly significant degree in mice, and the nasociliary nerves pass through the ciliary ganglia and extend alongside sections of the optic nerves. The cell bodies of ciliary ganglion and accessory ciliary ganglion neurons are also in contact with the optic nerves at sites rostral (anterior) to the point at which the oculomotor nerves intersect the optic nerves.

In any case, I never saw these articles because I never did searches on ultraviolet radiation in relation to the suprachiasmatic nucleus, etc. I only did searches on UVR's effects on the trigeminal system or on C-fibers/Adelta fibers and nociceptive transmission, etc.