High Frequency Oscillations are Phase-Amplitude Coupled in Stress Induced Seizures Following Traumatic Brain Injury
Abstract
Traumatic Brain Injury (TBI) often leads to the development of epilepsy, especially with the occurrence of stressful events. Stressors increase the levels of corticotropin-releasing factor (CRF) in the amygdala, which can be damaged by the secondary effects of TBI. It is hypothesized that the activity of CRF receptor type 1 (CRFR1) in the amygdala is altered post-TBI and supports the generation of epileptiform waves, namely high-frequency oscillations (HFOs). Sprague-Dawley rats were given a moderate TBI and in vivo recordings of the amygdala were taken during the administration of an acute tail pinch stressor. The stressor increased broadband activity which included the occurrence of HFOs. Moreover, HFO amplitudes were found to be coupled to the phase of a simultaneous theta wave (4 – 8Hz). Furthermore, application of a CRFR1 antagonist disrupted the generation of HFOs and their phase-amplitude coupling with theta, and these effects were reverted after washout of the antagonist.