Post-Injury Atomoxetine Treatment Improves Cognition following Experimental Traumatic Brain Injury

2008 ◽  
Vol 25 (3) ◽  
pp. 248-256 ◽  
Author(s):  
Wendy M. Reid ◽  
Robert J. Hamm
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Post Injury ◽  
Atomoxetine Treatment ◽  
Experimental Traumatic Brain Injury

scholarly journals Effects of Traumatic Brain Injury on Regional Cerebral Blood Flow in Rats as Measured with Radiolabeled Microspheres

1989 ◽  
Vol 9 (1) ◽  
pp. 117-124 ◽  
Author(s):  
Iwao Yamakami ◽  
Tracy K. McIntosh
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Brain Regions ◽  
Post Injury ◽  
Fluid Percussion ◽  
Hemodynamic Variables ◽  
Acute Changes ◽  
Injury Recovery ◽  
Left Parietal Cortex ◽  
Experimental Traumatic Brain Injury

To clarify the effect of experimental brain injury on regional CBF (rCBF), repeated rCBF measurements were performed using radiolabeled microspheres in rats Subjected to fluid-percussion traumatic brain injury. Three consecutive microsphere injections in six uninjured control rats substantiated that the procedure induces no significant changes in hemodynamic variables or rCBF. Animals were subjected to left parietal fluid-percussion brain injury of moderate severity (2.1–2.4 atm) and rCBF values were determined (a) prior to injury and 15 min and 1 h following injury (n = 7); and (b) prior to injury and 30 min and 2 h following injury (n = 7). At 15 min post injury, there was a profound reduction of rCBF in all brain regions studied (p < 0.01). Although rCBF in the hindbrain had recovered to near-normal by 30 min post injury, rCBF in both injured and contralateral (uninjured) forebrain areas remained significantly suppressed up to 1 h post injury. At 2 h post injury, recovery of rCBF to near-normal values was observed in all brain regions except the focal area of injury (left parietal cortex) where rCBF remained significantly depressed (p < 0.01). This prolonged focal oligemia at the injury site was associated with the development of reproducible cystic necrosis in the left parietotemporal cortex at 4 weeks post injury. Our results demonstrate that acute changes in rCBF occur following experimental traumatic brain injury in rats and that rCBF remains significantly depressed up to 2 h post injury in the area circumscribing the trauma site.

scholarly journals Changes in Neuropeptide Y after Experimental Traumatic Brain Injury in the Rat

1992 ◽  
Vol 12 (4) ◽  
pp. 697-702 ◽  
Author(s):  
Tracy K. McIntosh ◽  
Donna Ferriero
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Neuropeptide Y ◽  
Parietal Cortex ◽  
Brain Regions ◽  
Male Rats ◽  
Post Injury ◽  
Regional Brain ◽  
Left Parietal Cortex ◽  
Experimental Traumatic Brain Injury

We utilized a model of fluid percussion (FP) brain injury in the rat to examine the hypothesis that alterations in brain neuropeptide Y (NPY) concentrations occur following brain injury. Male rats (n = 44) were subjected to FP traumatic brain injury. One group of animals (n = 38) was killed at 1 min, 15 min, 1 h, or 24 h after brain injury, and regional brain homogenates were analyzed for NPY concentrations using radioimmunoassay. A second group of animals (n = 6) was killed for NPY immunocytochemistry. Concentrations of NPY in the injured left parietal cortex were significantly elevated at 15 min post injury (p < 0.05). No changes were observed in other brain regions. NPY-immunoreactive fibers were seen at 15 min post injury predominantly in the injured cortex and adjacent hippocampus. These temporal changes in NPY immunoreactivity, together with previous observations concerning posttraumatic changes in regional CBF in these same areas, suggest that an increase in region NPY concentrations after brain injury may be involved in part in the pathogenesis of posttraumatic hypoperfusion.

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