Authors :
Presenting Author: Robert Kotloski, MD PhD – WIlliam S Middleton Memorial Veterans Hospital
Yuzhen Pan, PhD – University of Wisconsin-Madison School of Medicine and Public Health
Rationale:
We hypothesized that the acute response to traumatic brain injury (TBI) shares mechanisms with brain plasticity in the kindling model. Utilizing two unique, complementary strains of inbred rats, selected to be either susceptible or resistant to seizure-induced plasticity evoked by kindling of the perforant path, we examined acute electrophysiological alterations in hippocampus and cortex after a moderate-to-severe brain injury.
Methods:
Perforant path kindling susceptible (PPKS) and perforant path kindling resistant (PPKR) rats were studied under urethane anesthesia. Wide-band recordings and single unit activity were collected from hippocampal fields including CA1, CA3, and the upper blade of the dentate granule cell layer (DGU), as well as layer V of overlying cortex (CTX). Recordings were performed immediately prior to a controlled cortical impact (CCI, 3mm impactor, 3mm depth, 6m/s velocity, 500msec dwell time) delivered to the contralateral cortex and immediately following injury. Signal analysis was performed on local field potentials and single unit activity, comparing across inbred strains, pre- and post-CCI, and across the recording sites. A statistical significance level of p< 0.05 was used for results reported below.