Paradoxical sleep

Measurement of movement of the eyeballs by means of electrodes placed adjacent to the eye sockets. The EOG parameter is important in defining REM sleep. Indeed, in animals sleep experiments where EOG data are not collected, the corresponding sleep state is most correctly termed paradoxical sleep. 

As we relax in preparation for and pass into sleep, the active desynchronised awake EEG characterised by the low-amplitude (5-10 pV) high-frequency (10-30 Hz) beta waves becomes progressively more synchronised giving larger (20-30 pV) and slower (8-12 Hz) alpha waves, and then even slower (1-4 Hz) and bigger (30-150 pV) delta waves. This so-called slow-wave sleep is interrupted at intervals of some 1-2h by the break-up and desynchronisation of the EEG into an awake-like pattern. Since this is accompanied by rapid eye movements, even though sleep persists and can be deeper, the phase is known as rapid eye movement, REM or paradoxical, sleep. It is a time when dreaming occurs and when memory may be secured. 

Boutrel, B, Franc, B, Hen, R, Hamon, M and Adrien, J (1999) Key role of 5-HTlB receptors in the regulation of paradoxical sleep as evidenced by 5-HTlB knock-out mice. J. Neurosci. 19 3204-3212. 

Boissard, R., Gervasoni, D., Schmidt, M. H. et al (2002). The rat ponto-medullary network responsible for paradoxical sleep onset and maintenance a combined microinjection and functional neuroanatomical study. Eur. J. Neurosci 16, 1959-73. 

Jones, B. E. (1991a). Paradoxical sleep and its chemical/structural substrates in the brain. Neuroscience 40, 637-56. 

Jouvet, M. (1988). The regulation of paradoxical sleep by the hypothalamo-hypophysis. Arch. Ital. Biol. 126, 259-74. 

Jouvet, M Vimont, P. Delorme, F. (1965). [Elective suppression of paradoxical sleep in the cat by monoamine oxidase inhibitors.]. C. R. Seances. Soc. Biol. Fil. 159,... 

Karczmar, A. G., Longo, V. G. De Carolis, A. S. (1970). A pharmacological model of paradoxical sleep the role of cholinergic and monoamine systems. Physiol. Behav. 5, 175-82. 

Sakai, K. Onoe, H. (1997). Critical role for M3 muscarinic receptors in paradoxical sleep generation in the cat. Eur. J. Neurosci 9, 415-23. 

Vanni-Mercier, G., Sakai, K., Lin, J. S. Jouvet, M. (1989). Mapping of cholinoceptive brainstem structures responsible for the generation of paradoxical sleep in the cat. Arch. ltal. Biol. 127, 133-64. 

Caballero, A. De Andres, I. (1986). Unilateral lesions in locus coeruleus area enhance paradoxical sleep. Electroencephalogr. Clin. Neurophysiol. 64, 339-46. 

Henley, K. 8r Morrison, A. R. (1974). A re-evaluation of the effects of lesions of the pontine tegmentum and locus coeruleus on phenomena of paradoxical sleep in the cat. Acta Neurobiol. Exp. (Wars). 34, 215-32. 

Jones, B. E. (1979). Elimination of paradoxical sleep by lesions of the pontine gigantocellular tegmental field in the cat. Neurosci. Lett. 13, 285-93. 

Jouvet, M. (1965). Paradoxical sleep - a study of its nature and mechanisms. Prog. Brain Res. 18, 20-62. 

Sakai, K. (1986). Central mechanisms of paradoxical sleep. Brain Dev. 8, 402-7. 

Sastre, J. P., Sakai, K. Jouvet, M. (1981). Are the gigantocellular tegmental field neurons responsible for paradoxical sleep Brain Res. 229, 147-61. 

Figure 4.1 Effect of an iontophoretic injection of bicuculline, a GABAa antagonist, on a locus coeruleus noradrenergic neuron. With reduced activity during slow wave sleep, this neuron then becomes silent during paradoxical sleep (PS). The application of bicuculline reversibly restores tonic discharge, indicating the role of GABA in the cessation of activity of this neuron during PS.

Figure 4.2 Model of the network responsible for paradoxical sleep onset and maintenance Abbreviations DRN, dorsal raphe nucleus 5-HT, serotonin LC, locus coeruleus NA, noradrenaline LDT, laterodorsal tegmental nucleus Ach, acetylcholine Me, magnocellular reticular nucleus Gly glycine DPMe, deep mesencephalic reticular nucleus PAG, periaqueductal gray DPGi, dorsal paragigantocellular reticular nucleus PPT, pedunculopontine nucleus PRN, pontine reticular nucleus SLD, sublaterodorsal nucleus Glu, glutamate Pef/HLA perifornical/lateral hypothalamic area Hcrt, hypocretin (i.e. orexin).

Boissard, R., Fort, P., Gervasoni, D., Barbagli, B. Luppi, P. H. (2003). Localization of the GABAergic and non-GABAergic neurons projecting to the sublaterodorsal nucleus and potentially gating paradoxical sleep onset. Eur. J. Neurosci. 18, 1627-39. 

Deurveilher, S., Hars, B. Hennevin, E. (1997). Pontine microinjection of carbachol does not reliably enhance paradoxical sleep in rats. Sleep 20, 593-607. 

Maloney, K. J., Mainvilie, L. Jones, B. E. (1999). Differential c-Fos expression in cholinergic, monoaminergic, and GABAergic cell groups of the pontomesencephalic tegmentum after paradoxical sleep deprivation and recovery. J. Neurosci 19, 3057-72. 

Sakai, K. (1985). Neurons responsible for paradoxical sleep. In Sleep Neurotransmitters and Neuromodulators, ed. A. Wauquier and Janssen Research Foundation. 

Sakai, K. Crochet, S. (2000). Serotonergic dorsal raphe neurons cease firing by disfacilitation during paradoxical sleep. Neuroreport 11, 3237-41. 

Sakai, K. Koyama, Y. (1996). Are there cholinergic and non-cholinergic paradoxical sleep-on neurones in the pons Neuroreport 7, 2449-53. 

Sakai, K., Sastre, J. P., Salvert, D. et al. (1979b). Tegmentoreticular projections with special reference to the muscular atonia during paradoxical sleep in the cat an HRP study. Brain Res. 176, 233-54. 

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