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Sleep-wake behavior is controlled by networks of neurons and neurotransmitters in the brain. There are multiple populations of wake-promoting neurons, but few sleep-promoting neurons have been identified. In this study, we revealed that the rostromedial tegmen-talnucleus, the GABAergic tail of the ventral tegmental area,regulates non-rapideye movement sleep. We show that neurons in the rat rostromedial tegmental nucleus, when activated by pharmacogenetics, increase and deepen non-rapid eye movement sleep. Inhibition of these neurons exhibits the opposite effects. Furthermore, rats with lesion…mehr

Produktbeschreibung
Sleep-wake behavior is controlled by networks of neurons and neurotransmitters in the brain. There are multiple populations of wake-promoting neurons, but few sleep-promoting neurons have been identified. In this study, we revealed that the rostromedial tegmen-talnucleus, the GABAergic tail of the ventral tegmental area,regulates non-rapideye movement sleep. We show that neurons in the rat rostromedial tegmental nucleus, when activated by pharmacogenetics, increase and deepen non-rapid eye movement sleep. Inhibition of these neurons exhibits the opposite effects. Furthermore, rats with lesion in the rostromedial tegmental nucleus have a reduced response of sleep homeostasis following sleep deprivation. We show that stimulation of the terminals of the neurons in the rostromedial tegmental nucleus inhibits dopaminergic neurons in the midbrain. Interestingly, inhibition of these dopaminergic neurons also has sleep-promoting effects. The current results provide a potential target forprolonging non-rapid eye movement sleep, improving sleep quality, and treating sleep disorders in dopamine-implicated mental illness.
Autorenporträt
Associate Professor of Pharmacology, School of Basic Medical Sciences, Fudan University. To study neuropsychopharmacology and sleep-wake regulation. Composed two pharmacology textbooks, respectively as Editor-in-chief or associate editor in chief.