Sleep researchers in different disciplines disagree about how fully dreaming can be explained in terms of brain physiology. Debate has focused on whether REM sleep dreaming is qualitatively different from nonREM (NREM) sleep and waking. A review of psychophysiological studies shows clear quantitative differences between REM and NREM mentation and between REM and waking mentation. Recent neuroimaging and neurophysiological studies also differentiate REM, NREM, and waking in features with phenomenological implications. Both evidence and theory suggest that there are isomorphisms between the phenomenology and the physiology of dreams. We present a three-dimensional model with specific examples from normally and abnormally changing conscious states.

/pdf/dreaming-and-the-brain-toward-a-cognitive-neuroscience-of-4pu7cg288c.pdf

Dreaming and the brain: toward a cognitive neuroscience of conscious states

Several theories claim that dreaming is a random by-product of REM sleep physiology and that it does not serve any natural function. Phenomenal dream content, however, is not as disorganized as such views imply. The form and content of dreams is not random but organized and selective: during dreaming, the brain constructs a complex model of the world in which certain types of elements, when compared to waking life, are underrepresented whereas others are over represented. Furthermore, dream content is consistently and powerfully modulated by certain types of waking experiences. On the basis of this evidence, I put forward the hypothesis that the biological function of dreaming is to simulate threatening events, and to rehearse threat perception and threat avoidance. To evaluate this hypothesis, we need to consider the original evolutionary context of dreaming and the possible traces it has left in the dream content of the present human population. In the ancestral environment human life was short and full of threats. Any behavioral advantage in dealing with highly dangerous events would have increased the probability of reproductive success. A dream-production mechanism that tends to select threatening waking events and simulate them over and over again in various combinations would have been valuable for the development and maintenance of threat-avoidance skills. Empirical evidence from normative dream content, children's dreams, recurrent dreams, nightmares, post traumatic dreams, and the dreams of hunter-gatherers indicates that our dream-production mechanisms are in fact specialized in the simulation of threatening events, and thus provides support to the threat simulation hypothesis of the function of dreaming.

https://www.unil.ch/files/live/sites/ln/files/shared/Revonsuo_1.pdf

The reinterpretation of dreams: An evolutionary hypothesis of the function of dreaming

Sleep and Dreaming: The reinterpretation of dreams: An evolutionary hypothesis of the function of dreaming

Neurochemical regulation of sleep

Sleep is regulated by homeostatic and circadian factors, and the regulation of sleep of mammals shares many molecular properties with the rest state of submammalian species. Several brain structures take part in waking: the basal forebrain, posterior and lateral hypothalamus, and nuclei in the tegmentum and pons. Active sleep mechanisms are located to the preoptic/anterior hypothalamic area. In addition to acetylcholine and monoamines, glutamate and hypocretin/orexin are important waking factors. Gamma-aminobutyric acid and several peptide factors, including cytokines, growth hormone-releasing hormone and prolactin, are related to sleep promotion. Adenosine is an important homeostatic sleep factor acting in basal forebrain and preoptic areas through A1 and A2A receptors. Prolonged waking activates inducible nitric oxide synthase in the basal forebrain, which through energy depletion causes adenosine release and recovery sleep. Numerous genes have been found differentially displayed in waking compared with sleep, and they relate to neural transmission, synaptic plasticity, energy metabolism and stress protection. The genetic background of a few sleep disorders has been solved.

Neuroanatomy and neurochemistry of sleep

Centrally administered vasoactive intestinal polypeptide (VIP) promotes rapid eye movement (REM) sleep in rats, rabbits, and cats. We studied the effect of 4 x 10 micrograms VIP (expt 1, n = 7) and 4 x 50 micrograms VIP (expt 2, n = 10) administered hourly as intravenous boluses between 2200 and 0100 on sleep electroencephalogram and secretion of plasma adreno corticotropic hormone, cortisol, growth hormone, and prolactin in humans. In experiment 2, the sleep cycles were decelerated during the first three cycles because of increased duration of both REM and non-REM sleep periods, and there was a tendency to increased REM-to-non-REM ratios. With a low VIP dose, prolactin levels were decreased during the whole night, whereas, with a high dose, they were increased during the first half of the night. In experiment 2, the cortisol nadir was advanced, after midnight the serum cortisol levels were enhanced, and the growth hormone peak was blunted. It appears that VIP may have a phase-advancing effect on sleep cycles and cortisol secretion, possibly through actions that involve the suprachiasmatic nucleus.

VIP decelerates non-REM-REM cycles and modulates hormone secretion during sleep in men

The neuropeptides growth hormone-releasing hormone (GHRH) and corticotropin-releasing hormone (CRH) play a key role in sleep endocrine regulation. After pulsatile application of GHRH during the first few hours of the night in young normal controls SWS and GH increase, whereas cortisol is blunted. CRH however prompts inverse effects. The balance between these peptides is changed in favour of CRH physiologically during the second time of the night, during the acute episode of depression (due to overactivity of GRH) and in the elderly (due to reduced activity of CHRH). These changes explain the aberrances of sleep endocrine activity in these states, as shallow sleep, low GH and enhanced cortisol.

Die Rolle von Neuropeptiden in der normalen und gestörten Schlafregulation

Die Ergebnisse aus Untersuchungen mit gesunden Kontrollpersonen [1] bzw. aus Tierexperimenten mit Ratten [2, 3] und Kaninchen [3] weisen darauf hin, das Wachstumshormon freisetzendes Hormon (GHRH) eine zentrale Rolle in der gemeinsamen Steuerung von hormoneller Sekretion und Schlaf spielt. So fuhren pulsatile, wahrend der ersten Nachthalfte erfolgende, intravenose GHRH-Injektionen bei gesunden jungen Mannern zu einer Steigerung von Tiefschlaf und Wachstumshormonausschuttung, wahrend die Cortisolausschuttung sinkt [1]. Moglicherweise tragt eine Hemmung der GHRH-Ausschuttung zu den fur Patienten mit Depression charakteristischen schlafendokrinologischen Auffalligkeiten bei. Gestorte Schlafkontinuitat, verminderter Tiefschlaf, verringerte Wachstumshormonsekretion und Hypercortisolismus sind haufige Symptome der Depression.

Die Effekte von Wachstumshormon freisetzendem Hormon (GHRH) auf hormonelle Sekretion und Schlaf-EEG bei depressiven Patienten

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VIP decelerates non-REM-REM cycles and modulates hormone secretion during sleep in men

Die Rolle von Neuropeptiden in der normalen und gestörten Schlafregulation

Die Effekte von Wachstumshormon freisetzendem Hormon (GHRH) auf hormonelle Sekretion und Schlaf-EEG bei depressiven Patienten