목적: Neural plasticity in the hippocampus has been suggested to occur after hearing loss. This study aimed to examine neural activation and excitatory signaling in the hippocampus (HC) and auditory cortex (AC) of hearing loss model rats by analyzing c-fos, vesicular glutamate transporter 1 (VGLUT1), parvalbumin (PV), and aggrecan (ACAN) expression. The implications for cognitive and emotional functions were also investigated. 방법: Bilateral ossicles were removed from four-week-old SD rats, and ouabain was applied to induce hearing loss. After two months, immunohistochemical (IHC) analysis was performed in the hippocampal CA1 and CA3 regions and the AC to evaluate the expression of VGLUT1, PV, and ACAN. The expression of cfos was examined after 90 minutes of broadband noise exposure (2–20 kHz, 80 dB SPL). The behavioral tests included the open field test (OFT) to assess total movement and center duration and the social interaction test (SIT) to evaluate social behavior and interaction time. 결과:Compared with control rats, hearing loss rats presented significant increases in c-fos expression in both the CA1 and CA3 regions. In addition, VGLUT1 expression was significantly elevated in the CA3 region, reflecting enhanced excitatory input. The expression of PV was similar to that in control rats, whereas the expression of ACAN was greater in hearing loss rats. In contrast, neither c-fos nor VGLUT1 expression significantly changed in the AC of hearing loss model rats. The expression of PV was similar to that in control rats, whereas the expression of ACAN was greater in hearing loss rats. Behavioral tests revealed that total movement in the OFT and SIT did not significantly differ between deaf and control rats. However, center duration in the OFT was significantly reduced, indicating increased anxiety-like behavior. Additionally, the SIT was markedly reduced despite unchanged overall movement, suggesting social avoidance behavior. 결론:The increases in c-fos in HCs indicate increased neuronal activity, suggesting that HCs compensate for sensory input loss through hyperactivation. Elevated VGLUT1 expression further supports increased excitatory signaling, potentially leading to an imbalance in excitatory-inhibitory regulation.