High expression of STIM1 in the early stages of diffuse axonal injury

Abstract

Increased intracellular calcium ([Ca(2+)](i)) is a key pathological mechanism involved in secondary neuronal injury and cell death due to diffuse axonal injury (DAI). To date, this increased [Ca(2+)](i) is believed to be mainly caused by dysfunction of voltage-gated sodium channels and mechanoporation of the plasma membrane. Store-operated calcium entry (SOCE) is another source of Ca(2+) influx, and stromal interaction molecule 1 (STIM1) is considered as a sensor and a regulator of SOCE. In this study, we established a DAI in vivo model in rats by lateral head rotation. Using immunohistochemistry, real-time RT-PCR and Western blot, we investigated STIM1 expression levels in the cerebral cortex of rats after lateral head rotational injury. Results revealed notably high STIM1 expression in neurons in the early stages (within 24 h) of DAI. STIM1 began to increase at 6 h post-injury (PI) peaked at 12 h PI, and then gradually decreased. At 2 days PI, STIM1 expression in the injury group showed no significant difference compared with that of the control group. These results indicate that abnormal SOCE may participate in Ca(2+) overload of neurons in the early stages after DAI via enhanced STIM1 expression.