OBJECTIVE:The aim of this study was to determine whether hyperbaric oxygen (HBO) therapy causes attenuation of traumatic brain injury (TBI)-induced depression-like behavior and its associated anti-neuroinflammatory effects after fluid percussion injury.
METHODS:Anesthetized male Sprague-Dawley rats were divided into three groups: sham operation + NBA (normobaric air: 21% O2 at 1 absolute atmosphere [ATA]), TBI + NBA, and TBI + HBO (100% O2 at 2.0 ATA). HBO was applied immediately for 60 min/day after TBI for 3 days. Depression-like behavior was tested by a forced-swimming test, motor function by an inclined plane test, and infarction volume by TTC staining on days 4, 8 and 15. Neuronal apoptosis (TUNEL assay), microglial (marker OX42) activation, and TNF-α expression in microglia in the hippocampus CA3 were measured by immunofluorescence methods.
RESULTS:Compared to the TBI controls, without significant changes in triphenyltetrazolium chloride (TTC) staining or in the motor function test, TBI-induced depression-like behavior was significantly attenuated by HBO therapy by day 15 after TBI. Simultaneously, TBI-induced neuronal apoptosis, microglial (marker OX42) activation, and TNF-α expression in the microglia in the hippocampus CA3 were significantly reduced by HBO.
CONCLUSIONS:Our results suggest that HBO treatment may ameliorate TBI-induced depression-like behavior in rats by attenuating neuroinflammation, representing one possible mechanism by which depression-like behavior recovery might occur. We also recommend HBO as a potential treatment for TBI-induced depression-like behavior if early intervention is possible.