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The employment of explosive weaponry in modern warfare exposes populations to shock wave-induced and impact-related brain injuries. Among the most common clinical complaints resulting from traumatic brain injury (TBI) are sleep-wake disturbances. The current study assessed the acute effects of mild concussive brain injury (CBI) and mild blast wave-induced brain injury (BTBI) on mouse behavior and orexin-A expression. Male C57BL/6J mice were exposed to CBI, BTBI, or sham procedures. Injured animals and their shams were further divided into the following subgroups: 24-h survival in standard group (SG) housing, 72-h survival in SG housing, and 72-h survival in Any-Maze cages (AMc). AMc enabled continuous monitoring of home cage activities. BTBI caused significant but transient decreases in wheel running and ingestive behaviors 24 h post-injury (PI), while CBI transiently decreased running and water intake. BTBI resulted in general hypoactivity in the open field (OF) at both PI time points for SG-housed animals. In contrast, CBI did not cause hypoactivity. Mice subjected to CBI traveled more in the center of the OF at both time points PI, suggesting that CBI caused reduced anxiety in mice. Increased activity in the center of the OF was also seen at 24 h PI after BTBI. CBI treatment caused increased CD11b immunostaining. However, neither injury was accompanied by an alteration in the number of orexin-A hypothalamic neurons. Taken together, shock wave exposure and concussive injury transiently reduced mouse activities, but some differences between the two injuries were seen.

Blast traumatic brain injury (bTBI) presents a serious threat to military personnel and often results in psychiatric conditions related to limbic system dysfunction. In this study, the functional outcomes for anxiety- and depressive-like behaviors and neuronal activation were evaluated in male and female mice after exposure to an Advanced Blast Simulator (ABS) shock wave. Mice were placed in a ventrally exposed orientation inside of the ABS test section and received primary and tertiary shock wave insults of approximately 15 psi peak pressure. Evans blue staining indicated cases of blood-brain barrier breach in the superficial cerebral cortex four, but not 24 h after blast, but the severity was variable. Behavioral testing with the elevated plus maze (EPM) or elevated zero maze (EZM), sucrose preference test (SPT), and tail suspension test (TST) or forced swim test (FST) were conducted 8 days–3.5 weeks after shock wave exposure. There was a sex difference, but no injury effect, for distance travelled in the EZM where female mice travelled significantly farther than males. The SPT and FST did not indicate group differences; however, injured mice were less immobile than sham mice during the TST; possibly indicating more agitated behavior. In a separate cohort of animals, the expression of the immediate early gene, c-Fos, was detected 4 h after undergoing bTBI or sham procedures. No differences in c-Fos expression were found in the cerebral cortex, but female mice in general displayed enhanced c-Fos activation in the paraventricular nucleus of the thalamus (PVT) compared to male mice. In the amygdala, more c-Fos-positive cells were observed in injured animals compared to sham mice. The observed sex differences in the PVT and c-Fos activation in the amygdala may correlate with the reported hyperactivity of females post-injury. This study demonstrates, albeit with mild effects, behavioral and neuronal activation correlates in female rodents after blast injury that could be relevant to the incidence of increased post-traumatic stress disorder in women.

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