Abstract: Objective To explore the effect of blocking of gap junction communication on neuronal apoptosis in rabbit hypothalamus after explosive brain injury. Methods Forty-eight rabbits were equally randomized into control group and experimental group. Octanol, a gap junction blocker, was injected through the left ventricle to block the gap junction communication in the experimental group and physiological saline in the control group instead. Rabbit models with explosive brain injury were induced by paper detonators 2 h after that. One, 3 and 7 d after the inducement, these rabbit models were sacrificed and thus, they were subdivided into 3 groups (n=8). The protein expression of gap junctional connexins 43 (Cx43) was observed by Western blotting and caspase-3 protein expressions in the hypothalamus were detected by immunohistochemical staining and RT-PCR. Results The protein expression of Cx43 in the experimental group was significantly lower than that in the control group at all time points (P<0.05), and that in the experimental group reached the peak level 3 d after the brain injury.The expressions of caspase-3 in the experimental group were significantly lower than those in the control group after the injury (P<0.05). Conclusion Blocking of gap junction communication can reduce the incidence rate of neuronal apoptosis in the hypothalamus after brain injury, and Cx43 might play an important regulation role in this process.