The full moon. Any bright night. A calendar curse.
A receptor in the hypothalamus fires at one wavelength only the full moon supplies. The adrenal surge follows.
The photobiological ignition key
Trigger · ipRGC–PVN axisPlate · LCAN · The photobiological ignition key · theoretical reconstruction
Light at about 415 nanometres hitting intrinsically photosensitive retinal ganglion cells, then the hypothalamus. That is the key, drawn as a circuit. The full moon is only the brightest, most reliable source of that band in a pre-electric night.
The moon does not emit. It reflects sunlight at an albedo of about 0.12 — at brightest, perhaps one three-hundred-thousandth of noon. Skin photobiology is not in play. The relevant photons are the ones that hit intrinsically photosensitive retinal ganglion cells, and the relevant geometry is opposition surge: only at full moon does zero-phase illumination produce a modest but documented excess at shorter visible wavelengths, around 410 to 415 nanometres, sitting on melanopsin's secondary shoulder.
encodes , a modified neuropeptide-Y-family receptor expressed not in the retina but in the paraventricular nucleus of the hypothalamus, and only in individuals whose LERV copy number and methylation state permit it. LR-1 is tuned to the downstream signal of that 415-nanometre ipRGC pulse. When it fires, the PVN dumps a CRH pulse eight to twelve times ordinary stress amplitude and, in parallel, a direct splanchnic volley to the adrenal medulla. Cortisol is the sideshow. The catecholamine surge is the ignition. Not a curse. A wavelength plus a receptor that should not exist.
Ch. 1
Werewolves in Theory