Neuronal networks and mechanisms responsible for sleep and their dysfunctions in pathologies
14 slide(s) – 00:20:59– English –2010-09-28
Since the discovery of rapid eye movement (REM) sleep (also known as paradoxical sleep; PS), it is accepted that sleep is an active process. PS is characterized by EEG rhythmic activity resembling that of waking with a disappearance of muscle tone and the occurrence of REMs, in contrast to slow-wave sleep (SWS, also known as non-REM sleep) identified by the presence of delta waves. I will describe an updated integrated model of the mechanisms responsible for the sleep-wake cycle. This model is based on results showing that the switch between waking and SWS is under the control of reciprocal interconnections between a population of SWS-active neurons located in the preoptic area and multiple waking systems. This model also introduces the notion that the entrance and exit of PS is induced by different mechanisms. I will hypothesize that the entrance from SWS to PS is due to the intrinsic activation of PS-on GABAergic neurons. These populations of neurons inhibit during PS all waking systems and a population of PS-off GABAergic neurons. This population of PS-off GABAergic neurons tonically inhibits during waking and SWS the glutamatergic neurons triggering the state of PS localized in the pontine sublaterodorsal tegmental nucleus (SLD). The exit from PS is induced by the inhibition of the PS-on GABAergic neurons by waking systems such as the pontine and medullary noradrenergic neurons and the hypothalamic hypocretin. Finally, I will propose hypotheses on the mechanisms responsible for two main sleep pathologies, REM sleep behaviour disorder and narcolepsy.