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Updated: Jan 15, 2026
Assessment of Memory Function in Pilocarpine-induced Epileptic Mice
Published on: June 4, 2020
Projections from prefrontal cortex to dorsal hippocampus mediate lipopolysaccharide induced recognition memory
Xin-Yu Zhao1, Jie Han1, Xin-Yi Cheng1
1NMPA Key Laboratory for Research and Evaluation of Narcotic and Psychotropic Drugs, Jiangsu Province Key Laboratory of Anesthesiology, Jiangsu Province Key Laboratory of Anesthesia and Analgesia Application, Xuzhou Medical University, 209 Tongshan Road, Xuzhou, Jiangsu, 221004, China.
Background:
s: Neuroinflammation plays a critical role in the development of cognitive impairment observed in postoperative patients. Meanwhile, the prefrontal cortex (PFC) and hippocampus are core brain regions that mediate learning and memory processes. However, the circuit mechanisms associated with the PFC and hippocampus that underlie neuroinflammation-induced cognitive dysfunction remain unclear.
Methods:
A mouse model of neuroinflammation was established via intraperitoneal injection of lipopolysaccharide (LPS). The object recognition task was employed to evaluate cognitive performance in mice. Fluorescent probe technology was used to record dynamic changes in glutamate and γ-aminobutyric acid (GABA) signaling within the PFC and the dorsal CA1 (dCA1) subregion of the hippocampus. Immunofluorescence assays were conducted to detect the activity of neurons in the mouse brain. Additionally, chemogenetic approaches were applied to manipulate the PFC-dCA1 neural pathway, thereby verifying its role in LPS-induced cognitive dysfunction.
Results:
LPS treatment significantly reduced the object recognition index in mice, accompanied by suppressed activity of GABAergic neurons in the PFC. Data from optical fiber recording revealed a marked decrease in GABA signaling received by dCA1 neurons in LPS-treated mice. Furthermore, chemogenetic activation of the PFC-dCA1 GABAergic projection pathway not only effectively promoted the performance of recognition memory in saline treated mice, but also relieved recognition memory impairment in LPS-treated mice.
Conclusion:
LPS-induced neuroinflammation triggers impaired recognition memory in mice through disrupting PFC-dCA1 functional connectivity, leading to decreased GABA signaling in the hippocampus. Enhancing PFC-dCA1 GABAergic pathway could relieve LPS-induced cognitive dysfunction, suggesting that this pathway may serve as a potential target in alleviating postoperative cognitive impairment.
