Store-operated calcium entry (SOCE) is crucial for cellular processes, including cellular calcium homeostasis and signaling. However, uncontrolled activation of SOCE is implicated in neurological disorders and CNS trauma, but underlying mechanisms remain unclear. We hypothesized that inhibiting SOCE enhances neurological recovery following contusive spinal cord injury (SCI). To investigate key SOCE effectors, stromal interaction molecules (STIM) and Orai channels on neurological recovery following spinal cord injury (SCI), we utilized male and female conditional neuronal Stim1KO mice to investigate the role of neuronal STIM1 in SCI outcome following a mild (30 kdyn) contusion at T13. To investigate Ca2+ store mediated Ca2+ store depletion, and SOCE-mediated refilling in SCI outcome, we inhibited the IP