Pleasure: The missing link in the regulation of sleep.

Although largely unrecognized by sleep scholars, sleeping is a pleasure. This report aims first, to fill the gap: sleep, like food, water and sex, is a primary reinforcer. The levels of extracellular mesolimbic dopamine show circadian oscillations and mark the "wanting" for pro-homeostatic stimuli. Further, the dopamine levels decrease during waking and are replenished during sleep, in opposition to sleep propensity. The wanting of sleep, therefore, may explain the homeostatic and circadian regulation of sleep. Accordingly, sleep onset occurs when the displeasure of excessive waking is maximal, coinciding with the minimal levels of mesolimbic dopamine. Reciprocally, sleep ends after having replenished the limbic dopamine levels. Given the direct relation between waking and mesolimbic dopamine, sleep must serve primarily to gain an efficient waking. Pleasant sleep (i.e. emotional sleep), can only exist in animals capable of feeling emotions. Therefore, although sleep-like states have been described in invertebrates and primitive vertebrates, the association sleep-pleasure clearly marks a difference between the sleep of homeothermic vertebrates and cool blooded animals.

Comments on evolution of sleep and the palliopallial connectivity in mammals and birds.

This commentary is referred to the review signed by Rattemborg [N.C. Rattenborg, Evolution of slow wave sleep and palliopallial connectivity in mammals and birds. A hypothesis. Brain Res. Bull. 69 (2006) 20-29]. We propose that the review missed important aspects in relation to the characteristics of sleep in poikilotherm vertebrates and in the evolution of sleep. Poikilotherms continuously show an EEG dominated by slow waves, but its highest amplitude appears not during sleep, but during active waking. In addition, they show an arousal reaction which consists in an increase in EEG amplitude and synchrony, opposite to mammals and birds. As a consequence, most of the conclusions proposed in the review should be rejected.

Why we sleep: the evolutionary pathway to the mammalian sleep.

The cause of sleep is a complex question, which needs first, a clear distinction amongst the different meanings of a causal relationship in the study of a given behavior, second, the requisites to be met by a suggested cause, and third, a precise definition of sleep to distinguish behavioral from polygraphic sleep. This review aims at clarifying the meaning of the question and at showing the phylogenetic origin of the mammalian and avian sleep. The phylogenetic appearance of sleep can be approached through a study of the evolution of the vertebrate brain. This began as an undifferentiated dorsal nerve, which was followed by the development of an anterior simplified brain and ended with the formation of the multilayered mammalian neocortex or the avian neostriate. The successive stages in the differentiation of the vertebrate brain produced, at least, two different waking types. The oldest one is the diurnal activity, bound to the light phase of the circadian cycle. Poikilotherms control the waking from the whole brainstem, where their main sensorymotor areas lie. Mammals developed the thalamocortical lines, which displaced the waking up to the cortex after acquiring homeothermy and nocturnal lifestyle. In order to avoid competence between duplicate systems, the early waking type, controlled from the brainstem, was suppressed, and by necessity was turned into inactivity, probably slow wave sleep. On the other hand, the nocturnal rest of poikilotherms most probably resulted in rapid eye movement sleep. The complex structure of the mammalian sleep should thus be considered an evolutionary remnant; the true acquisition of mammals is the cortical waking and not the sleep.

Dualism and uniformism in sleep.

The phenomenological evidence for distinguishing between REM and NREM sleep is overwhelming. However, this difference has only been found thanks to electrophysiological analytical methods, and is practically non existent in phenotypic terms, i.e., observable with the naked eye. It is well accepted that the selective pressure determining evolutionary changes can only work upon phenotypic differences. Hence, it follows that the differences between REM and NREM could not have been selected through evolution and this implies that, in functional terms, both states could be equivalent.

Thin-layer chromatographic determination of catecholamines, 5-hydroxytryptamine, and their metabolites in biological samples: a review.

A review of methodology for separation, detection, and quantitative determination of catecholamines, 5-hydroxytryptamine, and their acidic metabolites in biological tissue and fluids by thin-layer chromatography is presented. Selected procedures, including fluorometric scanning densitometry for catecholamine acetyl derivatives and color scanning densitometry for acids, are described.

Thin-layer chromatographic determination of catecholamines in rat plasma.

A TLC method for the quantitative determination of epinephrine, norepinephrine and dopamine in rat plasma is described. After deprotenization, catecholamines were adsorbed on acid-alumina and acetylated. The acetyl derivatives were extracted using a C18 minicolumn, resolved on HPTLC plates and quantitated by fluorescence densitometry at 415 nm, using isoprenaline as internal standard.