Journal
JOURNAL OF NEUROTRAUMA
Volume 25, Issue 11, Pages 1367-1374Publisher
MARY ANN LIEBERT, INC
DOI: 10.1089/neu.2008.0641
Keywords
anxiety; behavior; depression; rat; traumatic brain injury
Funding
- Victorian Government Transport Accident Commission [DP0023]
- National Health and Medical Research Council of Australia [400088]
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Mood disturbances, including depression and anxiety disorders, are common and disabling long-term sequelae of traumatic brain injury (TBI). These psychiatric conditions have generally been considered psychosocial consequences of the trauma, but neurobiological alterations and causes have also been implicated. Using a rat model of TBI (lateral fluid-percussion injury), this longitudinal study seeks to assess anxiety and depression-like behaviors following experimental TBI. Male Wistar rats (n=20) received a severe (similar to 3.5 atmosphere) pressure pulse directed to the right sensorimotor cortex, or sham surgery (n=15). At 1, 3, and 6 months following injury, all rats underwent four assessments of anxiety and depression-like behaviors: exposure to an open field, elevated plus maze test, the forced swim test, and the sucrose preference test. Injured animals displayed increased anxiety-like behaviors throughout the study, as evidenced by reduced time spent (p=0.014) and reduced entries (p<0.001) into the center area of the open field, and reduced proportion of time in the open arms of the plus maze (p=0.015), compared to sham-injured controls. These striking changes were particularly evident 1 and 3 months after injury. No differences were observed in depression-like behaviors in the forced swim test (a measure of behavioral despair) and the sucrose preference test (a measure of anhedonia). This report provides the first evidence of persistent anxiety-like disturbances in an experimental model of TBI. This finding indicates that the common occurrence of these symptoms in human sufferers is likely to have, at least in part, a neurobiological basis. Studies in this model could provide insight into the mechanisms underlying affective disturbance in brain-injured patients.
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