Postinjury Administration of l-Deprenyl Improves Cognitive Function and Enhances Neuroplasticity after Traumatic Brain Injury

摘要: The rat model of combined central fluid percussion traumatic brain injury (TBI) and bilateral entorhinal cortical lesion (BEC) produces profound, persistent cognitive deficits, sequelae associated with human TBI. In contrast to percussive TBI alone, this induces maladaptive hippocampal plasticity. Recent reports suggest a potential role for dopamine in CNS plasticity after trauma. We have examined the effect enhancer l-deprenyl on function neuroplasticity following Rats received TBI, BEC or + were treated once daily 7 days l-deprenyl, beginning 24 h alone 15 min BEC. Postinjury motor assessment showed no treatment. Cognitive performance was assessed 11-15 postinjury brains from same cases beta-hydroxylase immunoreactivity (DBH-IR) acetylcholinesterase (AChE) histochemistry. Significant improvement relative untreated injured observed both groups treatment; however, drug effects seen alone. l-Deprenyl attenuated injury-induced loss DBH-IR over CA1 CA3 However, BEC, only effective protecting DBH-IR. AChE histostaining significantly elevated models. After also increased dentate molecular layer cases. These results that dopaminergic/noradrenergic enhancement facilitates recovery noradrenergic fiber integrity is correlated enhanced synaptic hippocampus.