Abstract

AbstractBackgroundPostoperative cognitive dysfunction (POCD) is defined as a prolonged cognitive function impairment that occurs within weeks to months of a surgical procedure. Clinically this is a well‐known risk of the surgical experience in the elderly, having been described as a consequence of anesthesia. The medial prefrontal cortex (mPFC) plays a critical role in remote, recent, and short‐term memories over a broad range of tasks. The effect of POCD on neuronal plasticity in mPFC remains controversial. The present study investigates the impact of laparotomy on cognition and synaptic functions.MethodMice were induced with 5% sevoflurane and maintained with 3 ‐ 4% sevoflurane continuously for 30 mins. Under sevoflurane anesthesia, a 2.5 cm longitudinal midline incision was made. Approximately 10 cm of intestine was exteriorized and vigorously rubbed for 2 min and stay outside the abdominal cavity for 1 min. Novel Object Recognition (NOR) test was performed 1hour and 24 hours for the short‐term and long‐term memory seven days after the surgery. Open field test (OFT) and The Elevated Plus Maze test, was performed to exclude motor dysfunction and anxiety. The miniature excitatory postsynaptic currents (mEPSC) and miniature inhibitory postsynaptic currents (mIPSC) were recorded on the 7 or 14 days after surgery.ResultIn the NOR test, mice with undergone laparotomy surgery had worse cognitive performance than the control group. There was no significance between the laparotomy group and the control group in the OFT test and Elevated Plus Maze test. There was no significance in the amplitude of the mEPSC between laparotomy and control group. However, the frequency increased significantly in the laparotomy group than the control group, which can last for 14 days. There was no significance of mIPSC in the amplitude and frequency between the laparotomy group and the control group.ConclusionThese findings demonstrated that laparotomy surgery under sevoflurane leads to learning and memory impairment in adolescent mice without altering motor dysfunction and anxiety. The increase in the presynapse release ability indicated the glutamatergic neuron abnormalities without altering the GABAergic neuron’s function. Our result suggested that postoperative cognitive dysfunctions may be related to surgical trauma and glutamate neurons abnormalities.

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