Potential Role of Astrocyte Glycogen Depletion and "Supercompensation" to the Putative Circadian Neurobiological Effects of UVB Exposure

In reference to my previous posting, it's interesting that, apart from the neuronal pathways by which neurons in the caudal trigeminal nucleus could directly or indirectly influence hypothalamic neurons (there's quite a bit of research on the interactions of hypothalamic neurons with the trigeminal system in the context of migraines), activity in sensory neurons causes localized glycogen depletion in parts of the brain [Dienel et al., 2002: (http://www.nature.com/jcbfm/journal/v22/n12/full/9591343a.html)(http://www.ncbi.nlm.nih.gov/pubmed/12468893); (http://scholar.google.com/scholar?q=sensory+glycogen+stimulation&hl=en&lr=)]. That article showed an adaptive increase in glycogen content during "recovery" from the sensory stimulation, much as noradrenaline-induced astrocyte glycogen depletion is followed by a "rebound" increase in glycogen content (like a miniature version of glycogen "supercompensation" that can occur after glycogen-depleting exercise, when a person eats a high-carbohydrate diet, etc.). That could be an additional mechanism by which UVB exposure of the face, in particular, could regulate circadian neurobiology. Astrocyte glycogen levels (which constitute most of the brain glycogen) generally decrease progressively, during prolonged wakefulness, and UVB could intensify that pattern of glycogen depletion and overcompensation, etc., intensifying the entrainment of circadian neurobiological rhythms (http://scholar.google.com/scholar?num=100&hl=en&lr=&q=astrocyte+glycogen+sleep). The glycogen utilization, in the context of the asynchronous firing of trigeminal ganglion neurons, would produce depletion of astrocyte glycogen in various parts of the brain but could conceivably also participate in the subjective effects of UVB exposure. Maybe research on that type of mechanism would put all this business about "opioidergic" effects to rest.