Literature DB >> 1667742

Diffuse prolonged depression of cerebral oxidative metabolism following concussive brain injury in the rat: a cytochrome oxidase histochemistry study.

D A Hovda1, A Yoshino, T Kawamata, Y Katayama, D P Becker.   

Abstract

Utilizing a lateral fluid percussion injury as a model of cerebral concussion, rats were studied histochemically measuring the degree of cytochrome oxidase activity present within different structures at different times following injury. After concussion, the cerebral cortex ipsilateral to the site of injury exhibited a diffuse decrease in its level of chromotome oxidase (CO) activity beginning at as soon as one day and lasting for up to 10 days after the insult. The ipsilateral dorsal hippocampus also exhibited an injury-induced decrease in CO activity, however, it was not as severe as in the cortex. These results indicate that oxidative metabolism is depressed primarily within the cerebral cortex and hippocampus for several days following a cerebral concussion. We propose that this period of metabolic depression may delineate a period of time during which the injured brain is unable to function normally and thus would be vulnerable to a second insult.

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Year:  1991        PMID: 1667742     DOI: 10.1016/0006-8993(91)91429-5

Source DB:  PubMed          Journal:  Brain Res        ISSN: 0006-8993            Impact factor:   3.252


  52 in total

1.  Concussive brain injury enhances fear learning and excitatory processes in the amygdala.

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2.  Glucose administration after traumatic brain injury improves cerebral metabolism and reduces secondary neuronal injury.

Authors:  Nobuhiro Moro; Sima Ghavim; Neil G Harris; David A Hovda; Richard L Sutton
Journal:  Brain Res       Date:  2013-08-29       Impact factor: 3.252

3.  Traumatically injured astrocytes release a proteomic signature modulated by STAT3-dependent cell survival.

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4.  National Athletic Trainers' Association Position Statement: Management of Sport-Related Concussion.

Authors:  Kevin M Guskiewicz; Scott L Bruce; Robert C Cantu; Michael S Ferrara; James P Kelly; Michael McCrea; Margot Putukian; Tamara C Valovich McLeod
Journal:  J Athl Train       Date:  2004-09       Impact factor: 2.860

Review 5.  The combined effects of exercise and foods in preventing neurological and cognitive disorders.

Authors:  Fernando Gomez-Pinilla
Journal:  Prev Med       Date:  2011-01-31       Impact factor: 4.018

6.  Metabolic crisis without brain ischemia is common after traumatic brain injury: a combined microdialysis and positron emission tomography study.

Authors:  Paul Vespa; Marvin Bergsneider; Nayoa Hattori; Hsiao-Ming Wu; Sung-Cheng Huang; Neil A Martin; Thomas C Glenn; David L McArthur; David A Hovda
Journal:  J Cereb Blood Flow Metab       Date:  2005-06       Impact factor: 6.200

7.  Essential roles of neutral ceramidase and sphingosine in mitochondrial dysfunction due to traumatic brain injury.

Authors:  Sergei A Novgorodov; Christopher L Riley; Jin Yu; Keith T Borg; Yusuf A Hannun; Richard L Proia; Mark S Kindy; Tatyana I Gudz
Journal:  J Biol Chem       Date:  2014-03-21       Impact factor: 5.157

8.  Genetic activation of mTORC1 signaling worsens neurocognitive outcome after traumatic brain injury.

Authors:  Natalia S Rozas; John B Redell; Julia L Hill; James McKenna; Anthony N Moore; Michael J Gambello; Pramod K Dash
Journal:  J Neurotrauma       Date:  2014-12-10       Impact factor: 5.269

9.  The effects of a ketogenic diet on behavioral outcome after controlled cortical impact injury in the juvenile and adult rat.

Authors:  K Sofia Appelberg; David A Hovda; Mayumi L Prins
Journal:  J Neurotrauma       Date:  2009-04       Impact factor: 5.269

10.  Glucose administration after traumatic brain injury exerts some benefits and no adverse effects on behavioral and histological outcomes.

Authors:  Katsunori Shijo; Sima Ghavim; Neil G Harris; David A Hovda; Richard L Sutton
Journal:  Brain Res       Date:  2015-04-21       Impact factor: 3.252

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