It is no coincidence that the internal biological clock of most living things, from single-cell prokaryotes to humans, has a periodicity of approximately 24 hours. Obviously, evolution selected the species with a behavioral rhythm more or less synchronous to the rotation of the earth. Among all potential environmental factors on circadian rhythms, light was the first, and remains the most studied.
In about the middle of the 20th century it was demonstrated that the artificial administration of light stimulus on biological systems was able to induce a phase shift on circadian rhythm (3). The direction and the intensity of the shift changed according to when the stimulus was provided within the 24-hour day. The mathematical relationship between the time of light administration and the shift in the circadian system is graphically synthesized by the so-called phase-response curve (PRC) (4). The PRC shows that when the light stimulus is presented during the early subjective night it provokes a phase-delay shift, while the same stimulus presented in the late subjective night advances the circadian rhythm. The light effect during the subjective day is markedly reduced in some animals and, even abolished in others, during a time of the day known as the ''dead zone'' (5). Dark stimulus during the day usually has no effect. Until recently, several studies demonstrated that the experimental exposure to bright light induces phase shift on the majority of circadian biological phenomena, such as sleep, body temperature, MLT, and cortisol secretion (6-9).
According to the theory of the dose-response curve (DRC), the magnitude of the phase shift also depends, with nonlinear behavior, on the intrinsic characteristics of the light, such as the duration of exposure (10), the intensity of stimulus (11), and the spectral composition in terms of wavelength (12).
The majority of understanding regarding the mechanisms of light effect on animals remains unclear. The retina is a necessary target for light entrainment. Because PRC and DRC are also preserved in postchiasmatic blind people without conscious light perception, and even in different sightless experimental animals, it is likely that the photoreception apparatus accountable for these responses is distinct from that one responsible for the sensorial visual function (13-15). From these specialized cone photoreceptors the signal activates a pool of ganglion cells that project by the retinohypothalamic tract (RHT) to the SCN, and by the geniculohy-pothalamic tract (GHT) to the intergeniculate leaflet (IGL) of the thalamus (16). The RHT consists of monosynaptic glutamatergic neurons whose postsynaptic effect is mediated by N-methyl-d-aspartate (NMDA) and a-amino-5-hydroxy-3-methyl-4-isoxazole propionic acid receptors coupled with cyclic adenosine monophosphate (cAMP). Intracellular increases of calcium and cAMP in SCN cells results in a phosphorylation of nuclear DNA-binding proteins that regulate the transcription of specific genes. Reciprocal nervous connections between SCN and IGL nuclei have been demonstrated. Experimental lesions of RHT or GHT affect the light entrainment on circadian rhythm (17).
Although the strongest, light is not the only exogenous entrainment. Especially in human beings, food intake, locomotor activity, knowledge of the clock time, or different social cues, such as bedtime and work schedule, can reset the biological rhythms.
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