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• Vol.46 No.11
• CLINICA NEUROL, 46: 815−817, 2006
• Vol.46 No.11 contents

The 47th Annual Meeting of the Japanese Society of Neurology

Brain and sleep mechanism

Kunio Kitahama, M.D.

CNRS UMR 5123, Universiti Lyon I

It is now accepted that sleep is induced by biological clock located in the suprachiasmatic nucleus and/or sleep promoting substances, which influence ventrolateral preoptic (VLPO) neurons. The VLPO neurons affects more caudally situated posterior hypothalamic ones containing orexine and/or histamine, reciprocally. When these neurons inhibit lower brainstem aminergic ones, sleep is induced. REM (Rapid Eye Movement) sleep can be induced mainly by brainstem cholinergic neurons, when aminergic ones are completely inhibited. During this stage, tonic activities and phasic Ponto-Geniculate-Occipital (PGO) ones originated within brainstem cholinergic neurons activate irregularly many parts of the brain such as the cerebral cortex and limbic system to produce dream-like activity. Muscle atonia is also observed during REM sleep. This atonia is caused by neurons in the pontine reticular inhibitory area (PIA), which is normally inhibited by aminergic inputs. The PIA affects medullary neurons of the paramedian and/or magnocelullar nuclei to regulate motoneurons in the ventral horn. Therefore, muscle atonia is produced when these PPT cells are active during REM sleep. In addition, based upon many recent data, sleep is not a passive state but rather an active state, during which recuperation of neuronal system is promoted and information processing is executed.

(CLINICA NEUROL, 46: 815−817, 2006)
key words: Slow Wave Sleep, REM Sleep, Hypothalamus, Brain stem, Dream

(Received: 13-May-06)