There is an emerging body of literature suggesting that unlike the chronic neuroinflammatory response, acute neuroinflammation is self-regulated and is beneficial for central nervous system homeostasis and cognitive integrity. However, the neurophysiological alterations upon acute neuroinflammation and their implications on cognitive function remain poorly understood. In the present study, we reliably established a mouse model of acute and self-limiting neuroinflammation by administering a single intraperitoneal injection of low-dose lipopolysaccharide, which induced reversible sickness behavior and increased pro-inflammatory cytokine expression in the medial prefrontal cortex (mPFC). During acute neuroinflammation, fast-spiking parvalbumin-expressing interneurons (PV interneurons) in the mPFC exhibited a hyperexcitable phenotype exemplified by increased input resistance, decreased rheobase current, and a higher frequency of action potentials. Furthermore, PV interneurons in the prelimbic subregion of the mPFC were excessively recruited into circuits supporting novel object recognition memory, which remained intact after acute neuroinflammation. Together, our findings suggest that alterations in PV neuronal excitability resulting from acute neuroinflammation may mediate neuronal recruitment and confer a beneficial outcome on functional integrity of NOR circuit in the mPFC.

越来越多的文献表明，与慢性神经炎症反应不同，急性神经炎症是自我调节的，有利于中枢神经系统稳态和认知完整性。然而，对急性神经炎症的神经生理学改变及其对认知功能的影响仍然知之甚少。在本研究中，我们通过单次腹腔注射低剂量脂多糖可靠地建立了急性和自限性神经炎症的小鼠模型，该模型可诱导可逆的疾病行为并增加内侧前额叶皮层 (mPFC) 中促炎细胞因子的表达. 在急性神经炎症期间，mPFC 中表达快速尖峰小白蛋白的中间神经元 (PV 中间神经元) 表现出过度兴奋的表型，例如输入电阻增加、rheobase 电流降低和动作电位频率更高。此外，mPFC 前缘亚区的 PV 中间神经元被过度招募到支持新物体识别记忆的回路中，在急性神经炎症后保持完整。总之，我们的研究结果表明，由急性神经炎症引起的 PV 神经元兴奋性的改变可能介导神经元募集，并为 mPFC 中 NOR 回路的功能完整性带来有益的结果。mPFC 前缘亚区的 PV 中间神经元被过度招募到支持新物体识别记忆的回路中，在急性神经炎症后保持完整。总之，我们的研究结果表明，由急性神经炎症引起的 PV 神经元兴奋性的改变可能介导神经元募集，并为 mPFC 中 NOR 回路的功能完整性带来有益的结果。mPFC 前缘亚区的 PV 中间神经元被过度招募到支持新物体识别记忆的回路中，在急性神经炎症后保持完整。总之，我们的研究结果表明，由急性神经炎症引起的 PV 神经元兴奋性的改变可能介导神经元募集，并为 mPFC 中 NOR 回路的功能完整性带来有益的结果。