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Ronald L. Hayes, Bruce G. Lyeth, Larry W. Jenkins, Richard Zimmerman, Tracy K. McIntosh, Guy L. Clifton, and Harold F. Young

P revious research has indicated that traumatic brain injury (TBI) increases levels of endogenous opioids. Naloxone, a nonspecific opioid antagonist, significantly reverses the hypotension and reduction in pulse pressure following fluid-percussion injury in cats. 26 There are also recent clinical reports of increased µ -endorphin levels in the cerebrospinal fluid of head-injured patients. 80 Other laboratory studies have indicated that dynorphin A-immunoreactivity (but not leucine-enkephalin or µ -endorphin immunoreactivity) increased in the brain regions

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Grant Sinson, Brian R. Perri, John Q. Trojanowski, Eugene S. Flamm, and Tracy K. McIntosh

-percussion brain injury have been demonstrated months after injury. 20, 46 In the present study NGF administration significantly improved the ability of animals to learn a new task after traumatic brain injury (TBI). Loss of ipsilateral cortical and hippocampal CA3 pyramidal neurons is the most striking histological change in rodents undergoing lateral fluid-percussion brain injury. 3, 23 The identification of bilateral hippocampal cell loss in the region of the dentate hilus also suggests a potential mechanism underlying posttraumatic memory dysfunction in this model. 59

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Matthew F. Philips, Gustav Mattiasson, Tadeusz Wieloch, Anders Björklund, Barbro B. Johansson, Gregor Tomasevic, Alberto Martínez-Serrano, Philipp M. Lenzlinger, Grant Sinson, M. Sean Grady, and Tracy K. McIntosh

injury: a light and electron microscopic study in rats. J Neurotrauma 11 : 289 – 301 , 1994 Dietrich WD, Alonso O, Halley M: Early microvascular and neuronal consequences of traumatic brain injury: a light and electron microscopic study in rats. J Neurotrauma 11: 289–301, 1994 10. Dixon CE , Flinn P , Bao J , et al : Nerve growth factor attenuates cholinergic deficits following traumatic brain injury in rats. Exp Neurol 146 : 479 – 490 , 1997 Dixon CE, Flinn P, Bao J, et al: Nerve growth factor

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Grant Sinson, Madhu Voddi, and Tracy K. McIntosh

cholinergic cells into the hippocampus of rodents or primates following septohippocampal pathway lesions. 39, 54 Neural Transplantation After Traumatic Brain Injury The extracellular environment of the injured cortex may be hostile to cellular viability during the first 24 hours postinjury. 16, 49 Although transplants are more easily handled when they have been dissociated and placed in suspension, such treatment also exposes each cell to the pathological postinjury milieu. In the present study, the dissociation of fetal cells prior to transplantation resulted in

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Grant Sinson, Madhu Voddi, and Tracy K. McIntosh

This study was designed to evaluate the histological and behavioral impact of fetal neural transplantation with and without neurotrophin infusion in rats subjected to traumatic brain injury using a clinically relevant model of lateral fluid-percussion brain injury. Adult male Sprague-Dawley rats received lateral fluid-percussion brain injury of moderate severity (2.1-2.3 atm). Twenty-four hours after injury, minced fetal cortical grafts (E16) were stereotactically transplanted into the site of injury cavity formation (in 32 rats). Ten control animals received injections of saline. A third group of 29 animals that received transplants also underwent placement of a miniosmotic pump (immediately after transplantation) to continuously infuse nerve growth factor (NGF) directly into the region of graft placement for the duration of the experiment. A fourth group of eight animals underwent transplantation of fetal cortical cells that had been dissociated and placed in suspension. Animals were evaluated at 72 hours, 1 week, and 2 weeks after injury for cognitive function (using the Morris water maze), posttraumatic motor dysfunction, and transplant survival and morphology (using Nissl and modified Palmgren's silver staining techniques). Robust survival of whole-tissue transplants was seen in 65.6% of animals and was not increased in animals receiving NGF infusion. Animals receiving transplants of cell suspension had no surviving grafts. Brain-injured animals receiving transplants showed significant cognitive improvements compared with controls at the 2-week evaluation. Significantly improved memory scores were seen at all evaluation times in animals receiving both NGF and transplants compared with injured controls and compared with animals receiving transplants alone at the 72-hour and 1-week evaluations. Neurological motor function scores were significantly improved in animals receiving transplants alone and those receiving transplants with NGF infusion. Histological evaluation demonstrated differentiation of grafted cells, decreased glial scarring around transplants when compared with control animals, and the presence of neuronal fibers bridging the interface between graft and host. This study demonstrates that fetal cortical cells transplanted into the injured cortex of the adult rat can improve both posttraumatic cognitive and motor function and interact with the injured host brain.

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Koichi Okiyama, Douglas H. Smith, Mark J. Thomas, and Tracy K. McIntosh

T he calcium ion (Ca ++ ) may play a pivotal role in the pathogenesis of traumatic central nervous system (CNS) injury. It has been hypothesized that a massive increase in intracellular free calcium (Ca ++ i ) occurs after CNS injury. 10, 61, 62 This Ca ++ i overload may serve as the final pathway of irreversible neuronal damage in spinal cord injury, stroke, and traumatic brain injury. 45, 61, 62 An increase in Ca ++ i after brain injury could be caused by: 1) Ca ++ entry into cells via voltage-sensitive calcium channels; 2) the opening of excitatory

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Gregor Tomasevic, Helmut L. Laurer, Gustav Mattiasson, Harryvan Steeg, Tadeusz Wieloch, and Tracy K. McIntosh

DNA damage and regulate DNA repair processes, as well as activation of the DNA repair protein poly(adenosine diphosphate ribose) polymerase (PARP). 31 , 40 , 43 These findings indicate that DNA damage-related processes may play a role in the posttraumatic brain. To elucidate the possible role of an essential DNA repair protein in the pathogenesis of traumatic brain injury, we subjected genetically modified mice that lacked the XPA gene ( XPA −/− ) to CCI experimental brain trauma and compared the outcomes with those of wild-type mice ( XPA +/+ ). We

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Matthew F. Philips, Judith K. Muir, Kathryn E. Saatman, Ramesh Raghupathi, Virginia M.-Y. Lee, John Q. Trojanowski, and Tracy K. McIntosh

homeostasis and neuronal connectivity with restoration of function, 3, 20, 22, 42, 49, 50, 68 the potential benefit of CNS tissue transplantation for traumatic brain injury (TBI) has received relatively little attention. The pathological changes that occur as a result of lateral fluid-percussion injury (FPI) to the brain in rodents are similar to many changes that occur in human TBI. Injured brains of experimental animals exhibit both primary and secondary (delayed) neuronal death for a prolonged period after the traumatic event. 5, 19, 43, 60 Novel treatments for TBI are

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Kim M. Cecil, Everett C. Hills, M. Elizabeth Sandel, Douglas H. Smith, Tracy K. McIntosh, Lois J. Mannon, Grant P. Sinson, Linda J. Bagley, Robert I. Grossman, and Robert E. Lenkinski

D etection of white matter damage after traumatic brain injury (TBI) is important for the diagnosis, prognosis, and treatment of patients. Of particular significance is the white matter of the corpus callosum, because this commissure of the brain between cerebral hemispheres is exceptionally vulnerable to TBI. Although injury to the corpus callosum in patients suffering fatal injuries is routinely reported in the pathological literature, the detection of callosal injury remains underre-ported in the radiological and neurological literature for several reasons

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Niklas Marklund, Florence M. Bareyre, Nicolas C. Royo, Hilaire J. Thompson, Anis K. Mir, M. Sean Grady, Martin E. Schwab, and Tracy K. McIntosh

increase regeneration, plasticity and functional recovery of the lesioned central nervous system . Ann Med 37 : 556 – 567 , 2005 9 Cadelli D , Schwab ME : Regeneration of lesioned septohippocampal acetylcholinesterase-positive axons is improved by antibodies against the myelin-associated neurite growth inhibitors NI-35/250 . Eur J Neurosci 3 : 825 – 832 , 1991 10 Christman CW , Salvant JB , Walker SA , Povlishock JT : Characterization of a prolonged regenerative attempt by diffusely injured axons following traumatic brain injury in the adult