The trivial function of sleep.

Rest in poikilothermic animals is an adaptation of the organism to adjust to the geophysical cycles, a doubtless valuable function for all animals. In this review, we argue that the function of sleep could be trivial for mammals and birds because sleep does not provide additional advantages over simple rest. This conclusion can be reached by using the null hypothesis and parsimony arguments. First, we develop some theoretical and empirical considerations supporting the absence of specific effects after sleep deprivation. Then, we question the adaptive value of sleep traits by using non-coding DNA as a metaphor that shows that the complexity in the design is not a definitive proof of adaptation. We then propose that few, if any, phenotypic selectable traits do exist in sleep. Instead, the selection of efficient waking has been the major determinant of the most significant aspects in sleep structure. In addition, we suggest that the regulation of sleep is only a mechanism to enforce rest, a state that was challenged after the development of homeothermy. As a general conclusion, there is no direct answer to the problem of why we sleep; only an explanation of why such a complex set of mechanisms is used to perform what seems to be a simple function. This explanation should be reached by following the evolution of wakefulness rather than that of sleep. Sleep could have additional functions secondarily added to the trivial one, although, in this case, the necessity and sufficiency of these sleep functions should be demonstrated.

Effect of orally administered L-tryptophan on serotonin, melatonin, and the innate immune response in the rat.

To assess the effects of external administration of L-tryptophan on the synthesis of serotonin and melatonin as well as on the immune function of Wistar rats, 300 mg of the amino acid were administered through an oral cannula either during daylight (08:00) or at night (20:00) for 5 days. Brain, plasma, and peritoneal macrophage samples were collected 4 h after the administration. The accumulation of 5-hydroxytryptophan (5-HTP) after decarboxylase inhibition was used to measure the rate of tryptophan hydroxylation in vivo. Circulating melatonin levels were determined by radioimmunoassay, and the phagocytic activity of macrophages was measured by counting, under oil-immersion phase-contrast microscopy, the number of particles ingested. The results showed a diurnal increase (p < 0.05) in the brain 5-HTP, serotonin (5-hydroxytryptamine, 5-HT), and 5-hydroxyindolacetic acid (5-HIAA) of the animals which had received tryptophan at 08:00 and were killed 4 h later. In the animals which received tryptophan during the dark period, the 5-HT declined but the 5-HT/5-HIAA ratio remained unchanged. There was also a significant increase (p < 0.05) in nocturnal circulating melatonin levels and in the innate immune response of the peritoneal macrophages in the animals which had received tryptophan at 20:00. The results indicated that the synthesis of serotonin and melatonin, as well as the innate immune response, can be modulated by oral ingestion of tryptophan.