Trifluoperazine upregulates ACSS2-related autophagy and promotes cerebral cognitive function in rats after sleep
Caijun He1, Biao Wang1, Xuanyu Chen1
1The Second Affiliated Hospital, Department of Neurology, Hengyang Medical School, University of South China, Hengyang, Hunan 421001, China.
Abstract:
Cognitive function impairment following sleep deprivation (SD) can induce significant aftereffects. Elevated calmodulin (CaM) expression following stroke causes calcium overload-a key contributor to cognitive function impairment. Trifluoperazine (TFP), a CaM inhibitor, reduces CaM overexpression following ischemic stroke. However, it remains unclear whether TFP has influences on cognitive function impairment following SD. We administered TFP to rats subjected to SD. TFP treatment in SD rats reduced cerebral CaM expression and alleviated cognitive function impairment. Improved cognitive function was coincident with increased CaM protein levels and reduced acetyl-CoA synthetase 2 (ACSS2) protein levels after SD. TFP treatment reversed these changes. Our results showed that TFP administration in rats inhibited CaM protein following SD by upregulating ACSS2 protein expression, thereby improving ACSS2-related autophagy and alleviating cognitive function impairment. Consequently, this treatment may promote cerebral cognitive function recovery after SD.
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