Abstract
Vestibular impairment has become a frequent consequence following blast-related traumatic brain injury (bTBI) in military personnel and Veterans. Behavioral outcomes such as depression, fear and anxiety are also common comorbidities of bTBI. To accelerate pre-clinical research and therapy developments, there is a need to study the link between behavioral patterns and neuropathology. The transmission of neurosensory information often involves a pathway from the cerebral cortex to the thalamus, and the thalamus serves crucial integrative functions within vestibular processing. Pathways from the thalamus also connect with the amygdala, suggesting thalamic and amygdalar contributions to anxiolytic behavior. Here we used behavioral assays and immunohistochemistry to determine the sub-acute and early chronic effects of repeated blast exposure on the thalamic and amygdala nuclei. Behavioral results indicated vestibulomotor deficits at 1 and 3 weeks following repeated blast events. Anxiety-like behavior assessments depicted trending increases in the blast group. Astrogliosis and microglia activation were observed upon post-mortem pathological examination in the thalamic region, along with a limited glia response in the amygdala at 4 weeks. These findings are consistent with a diffuse glia response associated with bTBI and support the premise that dysfunction within the thalamic nuclei following repeated blast exposures contribute to vestibulomotor impairment.
Highlights
Neurosensory deficits such as vestibular impairment are a frequent outcome following traumatic brain injury (TBI) and if not treated can lead to long-term disability [1]
Over the 4 week period, there was no significant difference in the weights observed in the blast group when compared to the sham group
Elevated Levels of Microglia Found Within the Thalamus To identify areas of potential molecular mechanisms responsible for the observed vestibulomotor deficits, we examined the level of IBA-1 in three regions of the thalamus; central medial nuclei (CM), laterodorsal nuclei (LD), and ventrolateral nuclei (VL)
Summary
Neurosensory deficits such as vestibular impairment are a frequent outcome following traumatic brain injury (TBI) and if not treated can lead to long-term disability [1]. A report by Rusiecki et al measured serum levels of pro- and anti-inflammatory cytokines preand post-deployment of those who had been diagnosed with mild and moderate bTBI [40] They found chronic changes in several inflammatory markers (MMP3, IL-1α, IL-4, IL-6, and IL-8) indicating a long-term response to blast exposure. Preclinical studies show elevated levels of cytokines but extend to histological measures of neuroinflammation and reactive gliosis within animals exposed to blast events [41,42,43,44,45,46] These studies depict a significant contribution of neuroinflammation to the enduring complications of bTBI. We aimed to characterize neuropathological changes within the thalamus and amygdala following repeated blast exposures, providing more data to assist the mechanistic understanding of the vestibular impairment that presents clinically following a blast injury.
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