Treatment-resistant depression (TRD), which refers poor responses to adequate antidepressant treatment, have prominent cognitive impairment. Moreover, the depression patients with cognitive impairment could be a risk factor for dementia following aging. The lower aminobutyric acid type A receptor (GABAAR)-mediated activity and GABAB receptor (GABABR)-mediated activity was observed in prefrontal cortex (PFC) of patients with depression. Furthermore, the concentrations declined of both GABA in the PFC following the aging and at beginning of the mid-age has been found, suggesting the GABAergic system is highly associated with depression following aging. However, whether the GABAergic system involved in TRD-related cognitive decline following aging still unclear. In present study, we performed the TRD mice model which induced by traumatic stress in young- and mid-age mice. We applied the traumatic stress to induce the TRD symptom in mice model. The results indicated that depressive-like behavior was found after traumatic stress in both young- and mid-age mice. While, the cognitive impairment induced by traumatic stress was worse in mid-age mice. The aberrant dendritic morphology was observed after traumatic stress in both young- and mid-age mice. Moreover, the expression of GABAAR and GABABR were decreased after traumatic stress in both young- and mid-age mice. The depressive-like behavior was improved by GABAAR and GABABR activation. Whereas, the cognitive impairment did not improve by GABAAR and GABABR activation. Present study demonstrated the relationship between cognitive dysfunction and depression, especially TRD population, following aging. Furthermore, the evidences indicated GABAergic system only associates with depression, but not cognitive dysfunction following aging.