Citation

Eakin K, Miller JP. J. Neurotrauma 2012; 29(6): 1180-1187.

Affiliation

Cleveland, United States; Katharine.Eakin@case.edu.

Copyright

(Copyright © 2012, Mary Ann Liebert Publishers)

DOI

10.1089/neu.2011.2192

PMID

22229460

Abstract

Mild traumatic brain injury (mTBI) accounts for the majority of head trauma cases. Despite some lasting cognitive, emotional, and behavioral deficits, there are frequently no overt morphological defects, suggesting that changes may result from alterations in physiology of individual neurons. We investigated hippocampal neural activity in rats during a working memory task to determine the effect of mTBI on cellular physiology. Male Sprague-Dawley rats (300-350 g) underwent mTBI via lateral fluid percussion (1.5 atm) and were compared with sham-operated rats. Rats then underwent bilateral implantation of electrodes into the CA1 and CA3 hippocampal subfields and were trained to a delayed nonmatch-to-place swim T-maze. Single-neuron activity was analyzed during task performance 30-90 days after trauma. There were no histological differences between control and mTBI rats. Stereological analysis demonstrated no neuronal loss. Nevertheless, rats subjected to mTBI demonstrated significantly poorer performance on the task with increasing delay. Examination of single-neuron spiking activity revealed no significant difference in firing rates or spike characteristics, but rats exposed to mTBI were found to have significantly fewer cells with activity spatiotemporally correlated with location in the maze ("task-specific cells," p < 0.05, Fisher's exact test). Memory deficits, including disorganized patterns of hippocampal neural activity after mTBI, were seen in rats. Because it is seen in the absence of clear morphological defects, these data suggest that functional impairment after mTBI may result from alterations in activity of individual neurons.

Language: en