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Updated: Jun 12, 2026
Detecting Behavioral Deficits in Rats After Traumatic Brain Injury
Published on: January 30, 2018
Dexamethasone exacerbates spatial acquisition deficits after traumatic brain injury in rats
Xin Chen1, Yun-Peng Lin, Dong Wang
1Department of Neurosurgery, Tianjin Neurological Institute, General Hospital, Tianjin Medical University, Lab. of TJIVR, China.
Objectives:
Given after traumatic brain injury (TBI), Dexamethasone (DXM) reduces cerebral edema but impairs retrograde memory. This study was designed to test the hypothesis that administration of DXM to rats with TBI promotes learning deficits that are correlated with the morphological changes of hippocampal pyramidal neurons.
Methods:
Adult male Wistar rats were subjected to fluid percussion injury (FPI), received DXM (5 and 10 mg/kg), and then trained for spatial acquisition. Brain sections were examined by H.E. and Golgi impregnation to quantitatively measure the morphological changes of hippocampal pyramidal neurons.
Results:
The latency and path length were significantly higher in rats with FPI than those in control groups, particularly in rats receiving post-trauma high-dose DXM. At the same time, Golgi impregnation revealed a significant decrease in the number of apical and basal dendrites of pyramidal neurons of ipsilateral hippocampus in rats after injury, but the decrease was greatest of CA3 pyramidal neurons of ipsilateral hippocampus in injured rats that also received high-dose DXM.
Discussion:
These findings indicate that the administration of high-dose DXM after TBI could worsen the dendritic atrophy of hippocampal CA3 pyramidal neurons and, as a result, exacerbate spatial acquisition deficits.
