Temporal Pattern of Neurodegeneration, Programmed Cell Death, and Neuroplastic Responses in the Thalamus After Lateral Fluid Percussion Brain Injury in the Rat

The effects of traumatic brain injury (TBI) on the thalamus are not well characterized. We analyzed neuronal degeneration and loss, apoptosis, programmed cell death-executing pathways, and neuroplastic responses in the rat thalamus during the first week after lateral fluid percussion injury (LFPI). The most prominent neurodegenerative and neuroplastic changes were observed in the region containing the posterior thalamic nuclear group and ventral posteromedial and posterolateral thalamic nuclei ipsilateral to the LFPI. There was progressive neurodegeneration in these regions, with maximal neuronal loss on Day 7. Increases in numbers of apoptotic cells were detected on Day 1 and were enhanced on Days 3 and 7 after TBI. There was unchanged expression of active caspase-3 at all postinjury time points, but there was increased expression of apoptosis-inducing factor (AIF) on Day 7. The AIF nuclear translocation was detected on Day 1 and was maximal on Day 7. Total thalamic synaptophysin expression was unchanged, but immunostaining intensities were increased at all time points after TBI. Decreased growth-associated protein-43 expression and signal intensity were observed on Day 1. Our results suggest that progressive neuronal damage and loss, AIF signaling pathway-dependent programmed cell death, and limited neuroplastic changes occur in the rat thalamus during the first week after LFPI induction.