• Rosalia Paterno, Hannah Metheny, Guoxiang Xiong, Jaclynn Elkind, and Akiva S Cohen.
• 1 Center for Sleep and Circadian Neurobiology, Hospital of the University of Pennsylvania , Philadelphia, Pennsylvania.
• J. Neurotrauma. 2016 Sep 1; 33 (17): 1645-9.

AbstractCognitive impairment caused by traumatic brain injury (TBI) can lead to devastating consequences for both patients and their families. The underlying neurological basis for TBI-induced cognitive dysfunction remains unknown. However, many lines of research have implicated the hippocampus in the pathophysiology of TBI. In particular, past research has found that theta oscillations, long thought to be the electrophysiological basis of learning and memory, are decreased in the hippocampus post-TBI. Here, we recorded in vivo electrophysiological activity in the hippocampi of 16 mice, 8 of which had previously undergone a TBI. Consistent with previous data, we found that theta power in the hippocampus was decreased in TBI animals compared to sham controls; however, this effect was driven by changes in broadband power and not theta oscillations. This result suggests that broadband fluctuations in the hippocampal local field potential can be used as an electrophysiological surrogate of abnormal neurological activity post-TBI.

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