Faculty, Staff and Student Publications
Publication Date
11-1-2023
Journal
Journal of Neurotrauma
Abstract
The hippocampus plays a prominent role in learning and memory formation. The functional integrity of this structure is often compromised after traumatic brain injury (TBI), resulting in lasting cognitive dysfunction. The activity of hippocampal neurons, particularly place cells, is coordinated by local theta oscillations. Previous studies aimed at examining hippocampal theta oscillations after experimental TBI have reported disparate findings. Using a diffuse brain injury model, the lateral fluid percussion injury (FPI; 2.0 atm), we report a significant reduction in hippocampal theta power that persists for at least three weeks after injury. We questioned whether the behavioral deficit associated with this reduction of theta power can be overcome by optogenetically stimulating CA1 neurons at theta in brain injured rats. Our results show that memory impairments in brain injured animals could be reversed by optogenetically stimulating CA1 pyramidal neurons expressing channelrhodopsin (ChR2) during learning. In contrast, injured animals receiving a control virus (lacking ChR2) did not benefit from optostimulation. These results suggest that direct stimulation of CA1 pyramidal neurons at theta may be a viable option for enhancing memory after TBI.
Keywords
Rats, Animals, Optogenetics, Hippocampus, Pyramidal Cells, Brain, Neurons, Brain Injuries, Traumatic, Theta Rhythm, channelrhodopsin, fluid percussion injury, novel location, novel object recognition, theta stimulation
DOI
10.1089/neu.2023.0078
PMID
37387400
PMCID
PMC10653071
PubMedCentral® Posted Date
11-9-2023
PubMedCentral® Full Text Version
Post-print
Published Open-Access
yes