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Poster Display - 144
Dopamine D2 Receptor Modulating mPFC-BLA Circuitry Contributes to Chronic Sleep Deprivation-Induced Memory Impairment in Mice
Jiaxuan Yang 1, Xiaodong Liu 2, Yaoqin Hu 1, Jinpiao Zhu 1, Daqing Ma 1
1 Department of Anesthesiology, National Clinical Research Center for Child Health, The Children’s Hospital, Zhejiang University School of Medicine, Hangzhou, China,
2 Department of Anaesthesia and Intensive Care, The Chinese University of Hong Kong
Chronic sleep deprivation (CSD) affects neural networks leading to cognitive impairment but underlying molecular mechanisms remain unknown. Here, we reported that CSD in mice disinhibited dopaminergic input to the medial prefrontal cortex (mPFC) and impaired spatial memory. A significant increase of dopamine D2 receptor (Drd2) expression was found in layers II/III of the mPFC after CSD. Drd2 agonist applied to the mPFC reduced spatial memory in naïve mice while the Drd2 antagonist reversed CSD-induced deficits. Drd2 co-localized with Ca2+/calmodulin-dependent protein kinase IIa (CaMKIIa+) neurons in the mPFC projected to the basolateral amygdala (BLA). Activation of CaMKIIa+ neurons rescued memory impairment induced by CSD through enhancing output to the BLA and reversed memory defects induced by the Drd2 agonist. Our findings demonstrated that excessive Drd2 signaling after CSD suppresses mPFC-BLA neurotransmission leads to cognitive impairment, suggesting a possible therapeutic value of dopamine D2 receptor antagonists relieving CSD-induced cognitive decline.