Physiology of sleep
Although there is no evidence for a specific sleep ‘‘centre’’ in the brain, it is generally accepted that the level of consciousness is located in the diffuse network of nerve cells that comprise the reticular formation. This region consists of tegmental parts of the medulla, pons and midbrain. Lesions of the reticular formation result in somnolence or coma, sensory stimuli failing to arouse the animal. Such observations led to the conclusion that the brain stem reticular activity system maintains alertness and wakefulness, while lack of sensory stimulation results in sleep. Arousal from sleep by sensory stimuli is attributed to collateral pathways that link the main sensory pathways to the reticular formation. Undoubtedly this is a gross simplification of the anatomical substrate for sleep and wakefulness. There is evidence, for example, that animals may recover consciousness following lesions of the reticular formation and that the forebrain is not completely dependent on inputs from the reticular formation to maintain consciousness. Nevertheless, it is generally accepted that the reticular formation plays an important, if not a key role, in sleep and wakefulness.
Physiological basis of sleep – circadian rhythmicity It is a well-known fact that the circadian rhythm is entrained for diurnal cues to approximately 24 hours. However, a non-entrained rhythm, which operates in the absence of external cues, lasts between 25 and 27 hours. Thus the human sleep–wake cycle normally shows a 24-hour rhythm but not all physiological processes (for example, body temperature) follow the sleep–wake cycle. It is now known that circadian rhythms are controlled by clock genes which are found in species as wide apart as insects and mammals. It would appear that the clock genes are activated by light falling on the retina. The activated retina neurons then stimulate the retinohypothalamic tract which projects to the suprachiasmatic nucleus and thence to the anterior pituitary.
This pathway is responsible for coupling the circadian rhythm with the light cycle. The lateral geniculate nucleus (LGN) activates the suprachiasmatic nucleus (SCN) in the case of the non-light-based stimuli such as motor activity. The raphe´ nuclei also impact on the SCN. Thus several pathways appear to be involved in the entraining process.
Although there is no evidence for a specific sleep ‘‘centre’’ in the brain, it is generally accepted that the level of consciousness is located in the diffuse network of nerve cells that comprise the reticular formation. This region consists of tegmental parts of the medulla, pons and midbrain. Lesions of the reticular formation result in somnolence or coma, sensory stimuli failing to arouse the animal. Such observations led to the conclusion that the brain stem reticular activity system maintains alertness and wakefulness, while lack of sensory stimulation results in sleep. Arousal from sleep by sensory stimuli is attributed to collateral pathways that link the main sensory pathways to the reticular formation. Undoubtedly this is a gross simplification of the anatomical substrate for sleep and wakefulness. There is evidence, for example, that animals may recover consciousness following lesions of the reticular formation and that the forebrain is not completely dependent on inputs from the reticular formation to maintain consciousness. Nevertheless, it is generally accepted that the reticular formation plays an important, if not a key role, in sleep and wakefulness.
Physiological basis of sleep – circadian rhythmicity It is a well-known fact that the circadian rhythm is entrained for diurnal cues to approximately 24 hours. However, a non-entrained rhythm, which operates in the absence of external cues, lasts between 25 and 27 hours. Thus the human sleep–wake cycle normally shows a 24-hour rhythm but not all physiological processes (for example, body temperature) follow the sleep–wake cycle. It is now known that circadian rhythms are controlled by clock genes which are found in species as wide apart as insects and mammals. It would appear that the clock genes are activated by light falling on the retina. The activated retina neurons then stimulate the retinohypothalamic tract which projects to the suprachiasmatic nucleus and thence to the anterior pituitary.
This pathway is responsible for coupling the circadian rhythm with the light cycle. The lateral geniculate nucleus (LGN) activates the suprachiasmatic nucleus (SCN) in the case of the non-light-based stimuli such as motor activity. The raphe´ nuclei also impact on the SCN. Thus several pathways appear to be involved in the entraining process.
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