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Molecular Psychiatry (1997) 2, 195–196 1997 Stockton Press All rights reserved 1359–4184/97 $12.00 NEWS & VIEWS REM sleep and amygdala Recent PET data on human sleep suggest functional interactions between the amygdala and the cortex during REM sleep. This amygdalo-cortical interplay might reflect the processing of some types of memory traces. In humans, rapid eye movement (REM) sleep occurs in short periods recurring at regular intervals, mainly during the second half of the night. It is characterized by low-amplitude fast-frequency EEG waves, bursts of ocular saccades and muscular atonia. It is also strongly associated with dreaming. Since its discovery in the 1950s by Aserinky and Kleitman1 as well as Jouvet,2 REM sleep has been intensively investigated and a huge body of data has been collected in animals concerning its generation and maintenance at the cellular level.3 In short, cholinergic nuclei from the mesopontine reticular formation, liberated from the serotoninergic and noradrenergic inhibition, tonically activate the thalamic nuclei. In turn, these stimulate cortical areas. In particular, intralaminar thalamic nuclei project over and stimulate widespread cortical fields. This important neuronal activity explains why the global level of energy metabolism during REM sleep is comparable to the waking level.4,5 What is barely known is whether this diffuse telencephalic activation is homogeneous or not. In other words, the distribution of neuronal activity at the telencephalic level during REM sleep remains largely unexplored, especially in humans. Previous reports using PET or SPECT did not succeed in sketching a consistent metabolic pattern during REM sleep. Some authors described a significant metabolic increase in cingulate gyrus, corpus callosum and optic radiations. 6 Others observed an activation of posterior (occipital and temporal) areas during REM sleep, a metabolic pattern that was putatively attributed to dreaming activity.4,7 With the technological progress in PET methodology (H215O technique) and in data analysis (Statistical Parametric Mapping, SPM8), it has recently been possible to localize brain areas, whose activity characterizes REM sleep in humans.9 Experimental data show that some areas are more—and others less—activated than the rest of the brain. Not unexpectedly, an activation of dorsal pontine tegmentum and of thalamic nuclei was observed, consistent with data Correspondence: Dr P Maquet, Cyclotron Research Center (B30) and Department of Neurology, University of Liege, 4000 Liege, Belgium. E-mail: maquetKpet.crc.ulg.ac.be obtained in animals. More rostrally, an unexpected activation is shown in both amygdaloid complexes. Moreover, the distribution of cortical activity suggests that functional relationships take place between amygdala and the cortex during REM sleep. Indeed, significantly activated cortical areas (anterior cingulate cortex, parietal operculum) all receive a sizeable number of amygdalar connections (as can be inferred from what is known in primate neuroanatomy10) whereas the cortical regions with few or no amygdala afferents are significantly less active than the rest of the brain (prefrontal areas, parietal cortex, precuneus). From these results, one could speculate that, during REM sleep, the diffuse global activation of the cortex by central core structures (mesopontine reticular formation and thalami) is modulated by the amygdala. These results may further help to formulate some working hypotheses. First, amygdaloid complexes are known to associate an affective content to perceptions.11 They are also deeply involved in affective memory and experimental data further suggest that amygdala would modulate memory storage in other brain regions.12 On the other hand, both in animals and in man, REM sleep periods were shown to influence the consolidation of (mainly procedural) memory tasks.13 Taken together, these data suggest that the beneficial effect of REM sleep on some type of memory might, at least in part, rely on the modulation by amygdala of memory storage in other brain areas. Second, since all subjects recalled a dream after each REM sleep scan, these results also shed some light on the neural correlates of dreaming.14 One can speculate that the activation of the amygdala and anterior cingulate cortex could account for the emotional aspects of dreaming. The relative deactivation of some prefrontal areas could explain some of the aspects of dreams related to the loss of executive prefrontal functions: absence of strategy, poor critical introspection, distortion of temporal scale, amnesia upon awakening. The perceptual aspects of dreams would be brought about by the activation of various posterior cortices. Third, this study might provide some clues concerning the neural substrate of REM sleep disturbances in various pathologies such as narcolepsy and depression, News & Views 196 in which an amygdalar dysfunction has already been suggested. 15,16 There is still a lot of work to be done to test all these hypotheses in humans. However, we are confident that studies using coregistered functional neuroimaging techniques may be able to approach these questions in the near future. P Maquet, G Franck Cyclotron Research Center (B30) and Department of Neurology University of Liège 4000 Liège, Belgium References 1 Aserinski E, Kleitman N. 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