Objective:To explore the effects of vitamin D (VD) on lysosome activity and calcium channel protein Mcoln-1 in hippocampus and cortex of rats after traumatic brain injury (TBI).Methods:Forty-five SD rats were randomly divided into control group (Sham group), TBI model group (TBI group) and calcitriol treatment group (Calcitriol group). TBI models were established by electronic cortical impactor in TBI group and Calcitriol group. The rats in Calcitriol group were given of calitriol (1 μg/kg) by intraperitoneal injection at 30 min, 24 h and 48 h after TBI.Western blot was used to detect the expression of Mcoln-1, LAMP-1 and cathepsin-B in hippocampus and cortex region of rats. Immunofluorescence was used to detect the co-localization of Mcoln-1 and neurons three days later. Morris water maze test was performed on the 8th, 9th and 10th day after surgery in all groups.Results:Morris water maze results showed that compared with sham group((19.54±3.54)s, (18.64±4.63)s, (17.64±5.88)s), the latency of seeking platform escape ((58.75±6.65)s, (50.64±5.56)s, (42.64±5.87)s) were significantly increased in TBI group ( t=18.042, 14.325, 10.117; all P<0.05). On the 8th, 9th and 10th day after modeling, the escape latency of Calcitriol group((44.54±3.75)s, (30.74±4.74)s, (24.43±4.75)s)were significantly lower than those of TBI group ( t=6.539, 8.909, 7.369, all P<0.05). Western blot results showed that the expression of Mcoln-1 in cortex and hippocampus of TBI group were not significantly different from those of Sham group (both P>0.05). Compared with TBI group, the expression of Mcoln-1 protein in cortex and hippocampus of rats in Calcitriol group were significantly increased ( t=18.862, 17.336, both P<0.05). Immunofluorescence showed that the expression of Mcoln-1 and NeuN (neuron marker) co-located in the cortex and hippocampus of rats in the Calcitriol group. Conclusion:VD can improve learning and memory dysfunction after TBI in rats, and its mechanism may be related to the activation of Mcoln-1 calcium channel.