Delayed TBI-Induced Neuronal Death in the Ipsilateral Hippocampus and Behavioral Deficits in Rats: Influence of Corticosterone-Dependent Survivorship Bias?

Abstract

Acute and chronic corticosterone (CS) elevations after traumatic brain injury (TBI) may be involved in distant hippocampal damage and the development of late posttraumatic behavioral pathology. CS-dependent behavioral and morphological changes were studied 3 months after TBI induced by lateral fluid percussion in 51 male Sprague–Dawley rats. CS was measured in the background 3 and 7 days and 1, 2 and 3 months after TBI. Tests including open field, elevated plus maze, object location, new object recognition tests (NORT) and Barnes maze with reversal learning were used to assess behavioral changes in acute and late TBI periods. The elevation of CS on day 3 after TBI was accompanied by early CS-dependent objective memory impairments detected in NORT. Blood CS levels > 860 nmol/L predicted delayed mortality with an accuracy of 0.947. Ipsilateral neuronal loss in the hippocampal dentate gyrus, microgliosis in the contralateral dentate gyrus and bilateral thinning of hippocampal cell layers as well as delayed spatial memory deficits in the Barnes maze were revealed 3 months after TBI. Because only animals with moderate but not severe posttraumatic CS elevation survived, we suggest that moderate late posttraumatic morphological and behavioral deficits may be at least partially masked by CS-dependent survivorship bias.

Neuroprotective Effects of CXCR2 Antagonist SB332235 on Traumatic Brain Injury Through Suppressing NLRP3 Inflammasome

“…In this study, SB332235 was capable of ameliorating the neuronal damage and improved subsequent motor and cognitive de cits at 3 days post-injury. In parallel with previous studies [26, [33][34][35], our data showed that TBI caused pronouncedly higher mNSS score, reduction of time to maintain balance in beam-balance, enhancement in ambulatory time and a concomitant diminution in resting time in an open eld, and reduced discrimination index in novel object recognition task in animals, suggesting that TBI can trigger neurological de ciency, motor, and cognitive dysfunction. Of particular noteworthy, treatment with SB332235 potently reversed such de cits as shown by the lower mNSS score, elevation of time to maintain balance, decrease in ambulatory time and increase in resting time, and enhancement of discrimination index in TBI-exposed animals, indicative of a bene cial effect of SB332235 on the motor and memory impairments.…”

HBOT has a better cognitive outcome than NBH for patients with mild traumatic brain injury: A randomized controlled clinical trial

“…For the higher cognitive function of the brain, cognitive impairment will occur in multiple parts of either side, especially in functional areas such as frontal lobe and hippocampus. [ 19 ] Studies have shown that the cognitive impairment is more severe, especially the damage in the frontal lobe. Executive functions in the frontal lobe include abstract ability, concept formation, selective memory, and cognitive transfer processes.…”

TREM2 alleviates white matter injury after traumatic brain injury in mice might be mediated by regulation of DHCR24/LXR pathway in microglia

“…The spontaneous activities of mice in EPM were recorded for 5 min by ANY‐Maze software. The travelled time in the open arms and the total travelled distance were recorded and analyzed 35 …”