A Lateral Fluid Percussion Injury Model for Studying Traumatic Brain Injury in Rats

2018 ◽  
pp. 27-36 ◽  
Author(s):  
Paige S. Katz ◽  
Patricia E. Molina
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Fluid Percussion ◽  
Fluid Percussion Injury ◽  
Injury Model ◽  
Lateral Fluid Percussion

A rapid lateral fluid percussion injury rodent model of traumatic brain injury and post-traumatic epilepsy

Neuroreport ◽  
2014 ◽  
pp. 1 ◽  
Author(s):  
Mustafa Q. Hameed ◽  
Grant S. Goodrich ◽  
Sameer C. Dhamne ◽  
Asa Amandusson ◽  
Tsung-Hsun Hsieh ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Rodent Model ◽  
Fluid Percussion ◽  
Fluid Percussion Injury ◽  
Post Traumatic ◽  
Lateral Fluid Percussion ◽  
Post Traumatic Epilepsy ◽  
Traumatic Epilepsy

scholarly journals Harmonization of lateral fluid-percussion injury model production and post-injury monitoring in a preclinical multicenter biomarker discovery study on post-traumatic epileptogenesis

2019 ◽  
Vol 151 ◽  
pp. 7-16 ◽  
Author(s):  
Xavier Ekolle Ndode-Ekane ◽  
Cesar Santana-Gomez ◽  
Pablo M. Casillas-Espinosa ◽  
Idrish Ali ◽  
Rhys D. Brady ◽  
...  
Keyword(s):  
Biomarker Discovery ◽  
Post Injury ◽  
Fluid Percussion ◽  
Fluid Percussion Injury ◽  
Injury Model ◽  
Post Traumatic ◽  
Lateral Fluid Percussion

Hippocampal immediate early gene transcription in the rat fluid percussion traumatic brain injury model

Neuroreport ◽  
2014 ◽  
Vol 25 (12) ◽  
pp. 954-959 ◽  
Author(s):  
Yingpeng Wang ◽  
Mustafa Q. Hameed ◽  
Sanjay N. Rakhade ◽  
Antonio H. Iglesias ◽  
Paul A. Muller ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Gene Transcription ◽  
Immediate Early Gene ◽  
Early Gene ◽  
Immediate Early ◽  
Fluid Percussion ◽  
Traumatic Brain Injury Model ◽  
Injury Model

scholarly journals Implantation of Neuronal Stem Cells Enhances Object Recognition without Increasing Neurogenesis after Lateral Fluid Percussion Injury in Mice

2018 ◽  
Vol 2018 ◽  
pp. 1-11 ◽  
Author(s):  
Laura B. Ngwenya ◽  
Sarmistha Mazumder ◽  
Zachary R. Porter ◽  
Amy Minnema ◽  
Duane J. Oswald ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Stem Cell ◽  
Object Recognition ◽  
Brain Injury ◽  
Cell Transplantation ◽  
Hippocampal Neurogenesis ◽  
Cognitive Recovery ◽  
Fluid Percussion Injury ◽  
Immature Neurons ◽  
Lateral Fluid Percussion

Cognitive deficits after traumatic brain injury (TBI) are debilitating and contribute to the morbidity and loss of productivity of over 10 million people worldwide. Cell transplantation has been linked to enhanced cognitive function after experimental traumatic brain injury, yet the mechanism of recovery is poorly understood. Since the hippocampus is a critical structure for learning and memory, supports adult neurogenesis, and is particularly vulnerable after TBI, we hypothesized that stem cell transplantation after TBI enhances cognitive recovery by modulation of endogenous hippocampal neurogenesis. We performed lateral fluid percussion injury (LFPI) in adult mice and transplanted embryonic stem cell-derived neural progenitor cells (NPC). Our data confirm an injury-induced cognitive deficit in novel object recognition, a hippocampal-dependent learning task, which is reversed one week after NPC transplantation. While LFPI alone promotes hippocampal neurogenesis, as revealed by doublecortin immunolabeling of immature neurons, subsequent NPC transplantation prevents increased neurogenesis and is not associated with morphological maturation of endogenous injury-induced immature neurons. Thus, NPC transplantation enhances cognitive recovery early after LFPI without a concomitant increase in neuron numbers or maturation.

scholarly journals Hypothermia Attenuates the Loss of Hippocampal Microtubule-Associated Protein 2 (MAP2) following Traumatic Brain Injury

1993 ◽  
Vol 13 (5) ◽  
pp. 796-802 ◽  
Author(s):  
William C. Taft ◽  
Keyi Yang ◽  
C. Edward Dixon ◽  
Guy L. Clifton ◽  
Ronald L. Hayes
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Causal Link ◽  
Moderate Hypothermia ◽  
Post Injury ◽  
Protein Levels ◽  
Fluid Percussion ◽  
Fluid Percussion Injury ◽  
Neurobehavioral Deficits ◽  
Normothermic Group

Traumatic brain injury (TBI) produces a tissue-specific decrease in protein levels of microtubule-associated protein 2 (MAP2), an important cross-linking component of the neuronal cytoskeleton. Because moderate brain hypothermia (30°C) reduces certain neurobehavioral deficits produced by TBI, we examined the efficacy of moderate hypothermia (30°C) in reversing the TBI-induced loss of MAP2 protein. Naive, sham-injured, and moderate (2.1 atm) fluid percussion-injured rats were assessed for MAP2 protein content 3 h post injury using quantitative immunoreactivity measurements. Parallel groups of sham-injured and fluid percussion-injured animals were maintained in moderate hypothermia (30°C), as measured by temporalis muscle temperature, for MAP2 quantitation 3 h post injury. No difference in MAP2 levels was observed between naive and sham-injured normothermic animals. Hypothermia alone had no effect on soluble MAP2 levels in sham-injured animals compared with normothermic sham-injured controls (88.0 ± 7.3%; p > 0.10). Fluid percussion injury dramatically reduced MAP2 levels in he normothermic group (44.3 ± 5.9%; p < 0.0005) compared with normothermic sham-injured controls. No significant reduction of MAP2 was seen in the hypothermic injured group (95.2 ± 4.6%; compared with hypothermic sham-injured controls, p > 0.20). Although it is premature to infer any causal link, the data suggest that the attenuation of injury-induced MAP2 loss by hypothermia may contribute to its overall neuroprotective action.

Possible protective effect of endogenous opioids in traumatic brain injury

1990 ◽  
Vol 72 (2) ◽  
pp. 252-261 ◽  
Author(s):  
Ronald L. Hayes ◽  
Bruce G. Lyeth ◽  
Larry W. Jenkins ◽  
Richard Zimmerman ◽  
Tracy K. McIntosh ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Body Weight ◽  
Brain Injury ◽  
Endogenous Opioids ◽  
Neurological Deficits ◽  
Content Type ◽  
Fluid Percussion ◽  
Fluid Percussion Injury ◽  
Drug Treatments

✓ Naloxone (0.1, 1.0, or 20.0 mg/kg), morphine (1.0 or 10.0 mg/kg), or saline was administered systemically intraperitoneally to rats 15 minutes prior to moderate fluid-percussion brain injury. The effects of the drugs were measured on systemic physiological, neurological, and body-weight responses to injury. The animals were trained prior to injury and were assessed for 10 days after injury on body-weight responses and neurological endpoints. Low doses of naloxone (0.1 or 1.0 mg/kg) significantly exacerbated neurological deficits associated with injury. Morphine (10.0 mg/kg) significantly reduced neurological deficits associated with injury. The drugs had no effect on neurological measures or body weight in sham-injured animals. Drug treatments did not significantly alter systemic physiological responses to injury. Data from these experiments suggest the involvement of endogenous opioids in at least some components of neurological deficits following traumatic brain injury and suggest the possibility that at least some classes of endogenous opioids may protect against long-term neurological deficits produced by fluid-percussion injury to the rat.

Sign in / Sign up

Export Citation Format

Share Document