To further explore the molecular mechanisms by which the HPC-mPFC pathway regulates cognitive dysfunction in sepsis-induced brain injury, we used WB to examine the expression levels of AMPAR (GluA1, GluA2), NMDAR (NR1, NR2A/2B), and downstream signaling molecules including CaMKII, pCREB/CREB, BDNF, and TrKB in the mPFC (Figure 7A~D). Here, GRIN2A is linked to Sepsis.