2. Academic Validation
  3. Dexmedetomidine Promotes NREM Sleep by Depressing Oxytocin Neurons in the Paraventricular Nucleus in Mice

Dexmedetomidine Promotes NREM Sleep by Depressing Oxytocin Neurons in the Paraventricular Nucleus in Mice

  • Neurochem Res. 2024 Oct;49(10):2926-2939. doi: 10.1007/s11064-024-04221-w.
Ying Zhang # 1,  Jiaxin Li # 1,  Yan Li # 2,  Wei Wang 1,  Daming Wang 3,  Junli Ding 4,  Licheng Wang 5 6,  Juan Cheng 7
Affiliations

Affiliations

  • 1 Department of Physiology, School of Basic Medical Sciences, Anhui Medical University, Hefei, 230032, Anhui, China.
  • 2 Department of Pharmacy, Linquan People's Hospital, Linquan, 236400, Anhui, China.
  • 3 Department of Urology, The Second Affiliated Hospital of Anhui Medical University, Hefei, 230032, Anhui, China.
  • 4 Department of Pediatrics, First Affiliated Hospital of Anhui Medical University, Hefei, 230032, Anhui, China.
  • 5 Department of Physiology, School of Basic Medical Sciences, Anhui Medical University, Hefei, 230032, Anhui, China. wangliecheng@ahmu.edu.cn.
  • 6 College of Stomatology, Anhui Medical University, Hefei, 230032, Anhui, China. wangliecheng@ahmu.edu.cn.
  • 7 Department of Physiology, School of Basic Medical Sciences, Anhui Medical University, Hefei, 230032, Anhui, China. sophoscj12@163.com.
  • # Contributed equally.
PMID: 39078522 DOI: 10.1007/s11064-024-04221-w
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.

Keywords

DEX; EEG/EMG recording; Electrophysiological recording; OXT neurons; PVN.

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