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Dexmedetomidine Promotes NREM Sleep by Depressing Oxytocin Neurons in the Paraventricular Nucleus in Mice.
Zhang, Ying; Li, Jiaxin; Li, Yan; Wang, Wei; Wang, Daming; Ding, Junli; Wang, Licheng; Cheng, Juan.
Afiliación
  • Zhang Y; Department of Physiology, School of Basic Medical Sciences, Anhui Medical University, Hefei, 230032, Anhui, China.
  • Li J; Department of Physiology, School of Basic Medical Sciences, Anhui Medical University, Hefei, 230032, Anhui, China.
  • Li Y; Department of Pharmacy, Linquan People's Hospital, Linquan, 236400, Anhui, China.
  • Wang W; Department of Physiology, School of Basic Medical Sciences, Anhui Medical University, Hefei, 230032, Anhui, China.
  • Wang D; Department of Urology, The Second Affiliated Hospital of Anhui Medical University, Hefei, 230032, Anhui, China.
  • Ding J; Department of Pediatrics, First Affiliated Hospital of Anhui Medical University, Hefei, 230032, Anhui, China.
  • Wang L; Department of Physiology, School of Basic Medical Sciences, Anhui Medical University, Hefei, 230032, Anhui, China. wangliecheng@ahmu.edu.cn.
  • Cheng J; College of Stomatology, Anhui Medical University, Hefei, 230032, Anhui, China. wangliecheng@ahmu.edu.cn.
Neurochem Res ; 49(10): 2926-2939, 2024 Oct.
Article en En | MEDLINE | ID: mdl-39078522
ABSTRACT
Dexmedetomidine (DEX) is a highly selective α2-adrenoceptor agonist with sedative effects on sleep homeostasis. Oxytocin-expressing (OXT) neurons in the paraventricular nucleus (PVN) of the hypothalamus (PVNOXT) regulate sexual reproduction, drinking, sleep-wakefulness, and other instinctive behaviors. To investigate the effect of DEX on the activity and signal transmission of PVNOXT in regulating the sleep-wakefulness cycle. Here, we employed OXT-cre mice to selectively target and express the designer receptors exclusively activated by designer drugs (DREADD)-based chemogenetic tool hM3D(Gq) in PVNOXT neurons. Combining chemogenetic methods with electroencephalogram (EEG) /electromyogram (EMG) recordings, we found that cannula injection of DEX in PVN significantly increased the duration of non-rapid eye movement (NREM) sleep in mice. Furthermore, the chemogenetic activation of PVNOXT neurons using i.p. injection of clozapine N-oxide (CNO) after cannula injection of DEX to PVN led to a substantial increase in wakefulness. Electrophysiological results showed that DEX decreased the frequency of action potential (AP) and the spontaneous excitatory postsynaptic current (sEPSC) of PVNOXT neurons through α2-adrenoceptors. Therefore, these results identify that DEX promotes sleep and maintains sleep homeostasis by inhibiting PVNOXT neurons through the α2-adrenoceptor.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Núcleo Hipotalámico Paraventricular / Oxitocina / Dexmedetomidina / Neuronas Límite: Animals Idioma: En Revista: Neurochem Res Año: 2024 Tipo del documento: Article País de afiliación: China Pais de publicación: Estados Unidos

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Núcleo Hipotalámico Paraventricular / Oxitocina / Dexmedetomidina / Neuronas Límite: Animals Idioma: En Revista: Neurochem Res Año: 2024 Tipo del documento: Article País de afiliación: China Pais de publicación: Estados Unidos