The Increase in Local Cerebral Glucose Utilization Following Fluid Percussion Brain Injury is Prevented with Kynurenic Acid and is Associated with an Increase in Calcium

Hovda, David A.; Yoshino, Atsuo; Kawamata, Tatsuro; Katayama, Yoichi; Fineman, Igor; Becker, D. P.

doi:10.1007/978-3-7091-9115-6_112

Cited by 29 publications

(27 citation statements)

References 11 publications

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“…The phenomenon has been intensively studied after TBI in both humans and animals. 4,5,7,8 However, after SA it is unknown whether cerebral metabolism may change towards hyperglycolysis.…”

Section: Introductionmentioning

confidence: 98%

Cerebral energy failure after subarachnoid hemorrhage: The role of relative hyperglycolysis

Oertel

Schwedler

Stein

et al. 2007

Journal of Clinical Neuroscience

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“…The phenomenon has been intensively studied after TBI in both humans and animals. 4,5,7,8 However, after SA it is unknown whether cerebral metabolism may change towards hyperglycolysis.…”

Section: Introductionmentioning

confidence: 98%

Cerebral energy failure after subarachnoid hemorrhage: The role of relative hyperglycolysis

Oertel

Schwedler

Stein

et al. 2007

Journal of Clinical Neuroscience

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“…Based on the nature of primary injury following TBI, complex and heterogeneous secondary consequences result, which are followed by regenerative processes 1,2 . Primary injury can be induced by a direct contusion to the brain from skull fracture or from shearing and stretching of tissue causing displacement of brain due to movement 3,4 . The resulting hematomas and lacerations cause a vascular response 3,5 , and the morphological and functional damage of the white matter leads to diffuse axonal injury [6][7][8] .…”

Section: Introductionmentioning

confidence: 99%

“…Primary injury can be induced by a direct contusion to the brain from skull fracture or from shearing and stretching of tissue causing displacement of brain due to movement 3,4 . The resulting hematomas and lacerations cause a vascular response 3,5 , and the morphological and functional damage of the white matter leads to diffuse axonal injury [6][7][8] . Additional secondary changes commonly seen in the brain are edema and increased intracranial pressure 9 .…”

mentioning

confidence: 99%

Lateral Fluid Percussion: Model of Traumatic Brain Injury in Mice

Alder

Fujioka

Lifshitz

et al. 2011

JoVE

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Traumatic brain injury (TBI) research has attained renewed momentum due to the increasing awareness of head injuries, which result in morbidity and mortality. Based on the nature of primary injury following TBI, complex and heterogeneous secondary consequences result, which are followed by regenerative processes 1,2 . Primary injury can be induced by a direct contusion to the brain from skull fracture or from shearing and stretching of tissue causing displacement of brain due to movement 3,4 . The resulting hematomas and lacerations cause a vascular response 3,5 , and the morphological and functional damage of the white matter leads to diffuse axonal injury [6][7][8] . Additional secondary changes commonly seen in the brain are edema and increased intracranial pressure . Following TBI there are microscopic alterations in biochemical and physiological pathways involving the release of excitotoxic neurotransmitters, immune mediators and oxygen radicals [10][11][12] , which ultimately result in long-term neurological disabilities 13,14 . Thus choosing appropriate animal models of TBI that present similar cellular and molecular events in human and rodent TBI is critical for studying the mechanisms underlying injury and repair.Various experimental models of TBI have been developed to reproduce aspects of TBI observed in humans, among them three specific models are widely adapted for rodents: fluid percussion, cortical impact and weight drop/impact acceleration 1 . The fluid percussion device produces an injury through a craniectomy by applying a brief fluid pressure pulse on to the intact dura. The pulse is created by a pendulum striking the piston of a reservoir of fluid. The percussion produces brief displacement and deformation of neural tissue 1,15 . Conversely, cortical impact injury delivers mechanical energy to the intact dura via a rigid impactor under pneumatic pressure 16,17 . The weight drop/impact model is characterized by the fall of a rod with a specific mass on the closed skull 18 . Among the TBI models, LFP is the most established and commonly used model to evaluate mixed focal and diffuse brain injury 19. It is reproducible and is standardized to allow for the manipulation of injury parameters. LFP recapitulates injuries observed in humans, thus rendering it clinically relevant, and allows for exploration of novel therapeutics for clinical translation 20 .We describe the detailed protocol to perform LFP procedure in mice. The injury inflicted is mild to moderate, with brain regions such as cortex, hippocampus and corpus callosum being most vulnerable. Hippocampal and motor learning tasks are explored following LFP. Video LinkThe video component of this article can be found at https://www.jove.com/video/3063/ Protocol 1. Craniectomy 1. A sterile surgical site is prepared including a stereotaxic alignment instrument (Kopf Instruments) for mice with a mouse gas anesthesia head holder (Kopf Instruments) connected to an anesthesia machine with O 2 flush (Parkland Scientific) to allow for continuou...

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“…The ionic flux eventually leads to a metabolic mismatch in the acute period, as the mitochondria attempt to increase the production of ATP to meet the metabolic demands of the cell. The cell struggles to restore the ionic balance through activation of the ATP-dependent Na + -K + pump [28,29]. Trying to meet the energy demands, the cell activates glycolysis, producing lactate as a byproduct, which continues to accumulate due to disruption of the TCA cycle.…”

Section: Unchecked Neurotransmitter Releasementioning

confidence: 99%

The Pathophysiology of Concussion

Choe

2016

Curr Pain Headache Rep

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Concussion is a significant issue in medicine and the media today. With growing interest on the long-term effects of sports participation, it is important to understand what occurs in the brain after an impact of any degree. While some of the basic pathophysiology has been elucidated, much is still unknown about what happens in the brain after traumatic brain injury, particularly with milder injuries where no damage can be seen at the structural level on standard neuroimaging. Understanding the chain of events from a cellular level using studies investigating more severe injuries can help to drive research efforts in understanding the symptomatology that is seen in the acute phase after concussion, as well as point to mechanisms that may underlie persistent post-concussive symptoms. This review discusses the basic neuropathology that occurs after traumatic brain injury at the cellular level. We also present the pathology of chronic traumatic encephalopathy and its similarities to other neurodegenerative diseases. We conclude with recent imaging and biomarker findings looking at changes that may occur after repeated subconcussive blows, which may help to guide efforts in understanding if cumulative subconcussive mechanical forces upon the brain are detrimental in the long term or if concussive symptoms mark the threshold for brain injury.

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The Increase in Local Cerebral Glucose Utilization Following Fluid Percussion Brain Injury is Prevented with Kynurenic Acid and is Associated with an Increase in Calcium

Cited by 29 publications

References 11 publications

Cerebral energy failure after subarachnoid hemorrhage: The role of relative hyperglycolysis

Cerebral energy failure after subarachnoid hemorrhage: The role of relative hyperglycolysis

Lateral Fluid Percussion: Model of Traumatic Brain Injury in Mice

The Pathophysiology of Concussion

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