Objective To establish a mouse model of traumatic brain injury(TBI),to investigate the effects of visual cortex injury on neurobiology and cognitive function of the visual cortex.Methods Stereotaxic-guided graded cortical impacts(impact velocity was 1-4m/s)were administered to the primary visual cortex(V1)-associated skull surface in C57BL/6mice(8-week-old)with intact dura mater.Two weeks after the impact,the changes of neuronal numbers were analyzed by immunofluorescence staining and confocal mi-croscope imaging.Similar and 2-hour novel object recognition tests were used to evaluate the model visual function of mice.Open field tests and 24-hour novel object identification tests were used to assess the model non-visual abilities of mice,such as mobility,anxiety,and cognition.Results The number of superficial neurons in the mice's V1dropped by roughly 10％(P＜0.01)with an impact velocity of 4m/s,which was similar to what happens in individuals with mild brain injury.The recognition index(RI)of the TBI model mice was found to be significantly lower than that of the control group in the similar object recognition test(0.51±0.06 vs 0.58±0.05,P＜0.05).However,in the 2-hour novel object recognition test,no statistically significant difference in RI was detected between the TBI model mice and the control group(P＞0.05).Furthermore,the open field test indicated no significant disparities in locomotion speed or the time spent in the central area between the TBI model mice and the control group(P＞0.05).Similarly,the 24-hour novel object recognition test revealed no significant difference in RI between the TBI model mice and the control group(P＞0.05).Conclusion A mouse model simulating superficial injury to V1 was created through a controlled physical impact,characterized by a velocity of4m/s,a penetration depth of 0.5mm,and a dwell time of 0.5seconds.The visual capabilities of the model mice exhibited mild impairment,where-as their motor and cognitive functions remained intact.This model offers a novel research tool for exploring the mechanisms underlying the recovery of visual deficits following TBI.

Objective To establish a mouse model of traumatic brain injury(TBI),to investigate the effects of visual cortex injury on neurobiology and cognitive function of the visual cortex.Methods Stereotaxic-guided graded cortical impacts(impact velocity was 1-4m/s)were administered to the primary visual cortex(V1)-associated skull surface in C57BL/6mice(8-week-old)with intact dura mater.Two weeks after the impact,the changes of neuronal numbers were analyzed by immunofluorescence staining and confocal mi-croscope imaging.Similar and 2-hour novel object recognition tests were used to evaluate the model visual function of mice.Open field tests and 24-hour novel object identification tests were used to assess the model non-visual abilities of mice,such as mobility,anxiety,and cognition.Results The number of superficial neurons in the mice's V1dropped by roughly 10％(P＜0.01)with an impact velocity of 4m/s,which was similar to what happens in individuals with mild brain injury.The recognition index(RI)of the TBI model mice was found to be significantly lower than that of the control group in the similar object recognition test(0.51±0.06 vs 0.58±0.05,P＜0.05).However,in the 2-hour novel object recognition test,no statistically significant difference in RI was detected between the TBI model mice and the control group(P＞0.05).Furthermore,the open field test indicated no significant disparities in locomotion speed or the time spent in the central area between the TBI model mice and the control group(P＞0.05).Similarly,the 24-hour novel object recognition test revealed no significant difference in RI between the TBI model mice and the control group(P＞0.05).Conclusion A mouse model simulating superficial injury to V1 was created through a controlled physical impact,characterized by a velocity of4m/s,a penetration depth of 0.5mm,and a dwell time of 0.5seconds.The visual capabilities of the model mice exhibited mild impairment,where-as their motor and cognitive functions remained intact.This model offers a novel research tool for exploring the mechanisms underlying the recovery of visual deficits following TBI.