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Acute REM sleep deprivation alleviated depression-like behavior mediated by inhibiting VIP neurons in the mPFC

Yuxuan Zhu, Tongrui Wu, Qingyan Jiao, Haitong Chai, Yuang Wang, Chunxiao Tian, Qilin Xue, Kai Li, Pu Wang, Zhongchang Li, Hualin He, Bo Chen, Aili Liu, Hui Shen

2025Science Advances9 citationsDOIOpen Access PDF

Abstract

Acute sleep deprivation (SD) rapidly alleviates depression, addressing a critical gap in mood disorder treatment. Rapid eye movement SD (REM SD) modulates the excitability of vasoactive intestinal peptide (VIP) neurons, influencing the synaptic plasticity of pyramidal neurons. However, the precise mechanism remains undefined. To investigate this, we used a modified multiple platform method (MMPM) to induce 12 hours of REM SD, specifically targeting VIP neurons in the medial prefrontal cortex (mPFC). Our results show that REM SD mitigated depression by suppressing VIP neurons activity, which directly increased the excitability of pyramidal neurons and, consequently, promoted synaptic plasticity recovery. In addition, the knockdown of VPAC2 on mPFC pyramidal neurons revealed that VPAC2-mediated AC/cAMP/PKA signaling pathway in these neurons is essential for REM SD to mitigate depression-like behavior. These findings suggest that VIP neurons directly regulate pyramidal neurons and are crucial in alleviating depression by REM SD.

Topics & Concepts

Vasoactive intestinal peptideNeurosciencePrefrontal cortexSynaptic plasticityGene knockdownNeuroplasticitySleep deprivationSleep (system call)MedicineEndocrinologyNeuroscience of sleepInternal medicineRapid eye movement sleepMoodDendritic spineNAV1Cortical neuronsPsychologySynapseBiologyDepression (economics)NeurotransmitterNeuropeptideNeurotransmissionMechanism (biology)PlasticityChemistryElectrophysiologyPrivationNeuronSleep and Wakefulness ResearchCircadian rhythm and melatoninNeuroscience of respiration and sleep