Injured Fluoro-Jade-positive hippocampal neurons contain high levels of zinc after traumatic brain injury.

Hippocampal damage contributes to cognitive dysfunction after traumatic brain injury (TBI). We previously showed that Fluoro-Jade, a fluorescent stain that labels injured, degenerating brain neurons, quantifies the extent of hippocampal injury after experimental fluid percussion TBI in rats. Coincidentally, we observed that injured neurons in the rat hippocampus also stained with Newport Green, a fluorescent dye specific for free ionic zinc.

Molecular correlates of age-specific responses to traumatic brain injury in mice.

Aged traumatic brain injury (TBI) patients suffer higher rates of mortality and disability than younger patients. Cognitive problems common to TBI patients are associated with damage to the hippocampus, a central locus of learning and memory. To investigate the molecular mechanisms of age-related vulnerability to brain injury in a mouse model of TBI, we studied the effects of TBI on hippocampal gene expression in young and aged mice.

Traumatic brain injury and hemorrhagic hypotension suppress neuroprotective gene expression in injured hippocampal neurons.

Background: After traumatic brain injury, memory dysfunction is due in part to damage to the hippocampus. To study the molecular mechanisms of this selective vulnerability, the authors used laser capture microdissection of neurons stained with Fluoro-Jade to directly compare gene expression in injured (Fluoro-Jade-positive) and adjacent uninjured (Fluoro-Jade-negative) rat hippocampal neurons after traumatic brain injury and traumatic brain injury plus hemorrhagic hypotension.

Methods: Twelve isoflurane-anesthetized Sprague-Dawley rats underwent moderate (2.

Laser capture microdissection and analysis of amplified antisense RNA from distinct cell populations of the young and aged rat brain: effect of traumatic brain injury on hippocampal gene expression.

To explore the molecular mechanisms underlying the increased vulnerability of the aged brain to traumatic brain injury (TBI), we compared the expression of several age-related genes in the CA1, CA3 and dentate gyrus subfields of the young and aged rat hippocampus before and after lateral fluid percussion TBI. Using laser capture microdissection (LCM), we obtained hippocampal neurons and glia from the neuropil adjacent to the pyramidal and granule cell layers. Subsequently, we linearly amplified and analyzed the antisense mRNA using Northern blot and ribonuclease protection assays (RPA).