Traumatic brain injury (TBI) is a neurological event where an external mechanical force to the brain can lead to devastating effects on physical, cognitive, and/or behavioural function in humans. Currently, no therapeutic approach is substantially efficient in treating prolonged secondary injury from TBI. Deep brain stimulation (DBS) is a neurosurgical procedure used tomanage debilitating symptoms in motor disorders. While DBS is demonstrated to modulate targeted brain circuitry, its underlying mode of action is yet to be determined. This thesis hypothesizes that high-frequency acute DBS delivered to the anterior thalamic nucleus (ANT) will lead to recovery of memory deficits and reduce anxiety-type behaviour in a well-established TBI rodent model, through a decrease in apoptosis. Salient findings suggest: (i) Acute stimulation of the ANT improved spatial memory in rats with moderate-to-severe TBI, compared to rats receiving no DBS; however, (ii) anti-apoptotic effects after ANT-DBS, as assessed via caspase-3 measurements, were inconclusive.