Objective: To make a mouse model of traumatic spinal cord injury (SCI) by Allen's weight dropping (WD), which might be helpful for further research on the mechanism of SCI.
Methods: A total of 180 healthy female mice, weighing 17 - 23 g (20 g on average), were randomized into 4 groups (n=45 per group): the experimental groups of A, B and C and the control group of D. Experimental groups were distinguished by the amount of weight or the height from which the weight was dropped onto an impounded resting on the dura (2.0 x 2.5 g cm, 2.5 x 3.0 g cm, 3.0 x 5.0 g cm). In group D, neural scute was opened only and spinal cord was exposed without SCI. The recovery of the lower extremity was observed at various time points (0, 6 and 12 hours, 1 and 3 days, 1, 2, 4 and 8 weeks) by using the Basso mouse scale (BMS) scoring system, motor evoked potentials (MEP) and histological observation.
Results: MEP displayed that the incubation period of N1 wave was extended in group B after 6 hours and in group C after 12 hours. As time passed by, the incubation periods of N1 wave in group A, group B and group C began to shorten. The incubation period in group A was close to normal at 4 weeks (2.40 +/- 0.12) ms, and there was no significant difference compared with group D (P > 0.05). The incubation period in group B was close to normal at 8 weeks (2.96 +/- 0.15) ms, and there was no significant difference compared with group D (P > 0.05). The incubation period in group C was still relatively high at 8 weeks (3.76 +/- 0.13) ms, and there was a significant difference compared with group D (P < 0.05). Both hind limbs of all mice were paralytic instantly after SCI, the score of main BMS was 0 point; the score of main BMS was close to 0 at the first 3 days after SCI, the score of main BMS of group A was 8.00 +/- 0.13 and group B was 7.50 +/- 0.31 at 8 weeks; the score of main BMS of group A was 5.45 +/- 0.12 at 1 week and group B was 5.45 +/- 0.15 at 2 weeks which were significant difference compared with group D (P < 0.05).There were significant differences among groups A, B and C after 1 week of SCI (P < 0.05), and group C was lower than the others(P < 0.01). The score of adjuvant BMS of group A was 10.12 +/- 0.76 at 2 weeks and group B was 9.85 +/- 0.55 at 8 weeks which was no significant difference compared with the group D at the same time (P > 0.05). Histological observation showed hemorrhage, cellular edema, inflammatory cell infiltration, nerve cell swell and solution of Nissl body 12 hours after SCI in group C. As time passed by, the number of nerve cells decreased, the glial cell proliferated and Nissl body vanished. There was much glial cell proliferation and cavitation 2 weeks after SCI in group C. The nerve cell decrease and cavitation in group B was slighter than that in group C, and group A was the slightest. In group D, there was no obvious change of the number of cells during the observation apart from slight edema in early period.
Conclusion: The mouse model precisely reflects the pathological and physiological features and law of change after different degrees of SCI, and can be used as a standard of mouse model of traumatic SCI by Allen's WD.