DESCRIPTION (provided by applicant): In the United States alone, 500,000 people suffer traumatic brain injury (TBI) annually, making TBI a leading cause of death and disability. With improved accident scene and emergency care, mortality rates have declined, with 2-4 million people surviving TBI. Patients and patient families chiefly complain about post-concussive syndrome, involving alterations in cognition, aggression, emotional stability, disinhibition, and personality. In fact, post-concussive syndrome resembles the symptoms of amygdala resection or degeneration. In light of these post-injury deficits, the proposed project initiates experimentation focused on whether a subset of symptoms that define post-concussion syndrome are mediated by damage to the amygdala in a clinically relevant lateral fluid percussion model of brain injury in the mouse. The central hypothesis is: experimental TBI damages the amygdala bilaterally. Three aims test the hypothesis: (1) to demonstrate amygdala-dependent cognitive deficits using conditioned fear, (2) to quantify selective neuronal loss in the basolateral complex and central nucleus of the amygdala using design-based stereology, and (3) to evaluate and pharmacologically modulate functional circuitry and synaptic plasticity in the amygdala-hippocampal circuit using extracellular field recordings. The systems approach to investigate amygdala pathology after TBI, in terms of behavior, anatomy and function, can reveal mechanisms underlying post-concussion syndrome. This research effort may lead to novel treatments for the affective disorders in an otherwise healthy brain-injured population, in addition to post-traumatic stress disorder and psychosis.
|Effective start/end date||9/20/04 → 9/19/06|
- National Institutes of Health: $48,928.00
- National Institutes of Health: $51,548.00
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