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Titolo:
A new model for diffuse brain injury by rotational acceleration: II. Effects on extracellular glutamate, intracranial pressure, and neuronal apoptosis
Autore:
Runnerstam, M; Bao, F; Huang, YL; Shi, JS; Gutierrez, E; Hamberger, A; Hansson, HA; Viano, D; Haglid, K;
Indirizzi:
Univ Gothenburg, Dept Anat & Cell Biol, SE-40530 Gothenburg, Sweden Univ Gothenburg Gothenburg Sweden SE-40530 , SE-40530 Gothenburg, Sweden Chalmers Univ Technol, Crash Safety Div, S-41296 Gothenburg, Sweden Chalmers Univ Technol Gothenburg Sweden S-41296 41296 Gothenburg, Sweden Sahlgrens Univ Hosp, Dept Neurosurg, S-41345 Gothenburg, Sweden Sahlgrens Univ Hosp Gothenburg Sweden S-41345 S-41345 Gothenburg, Sweden China Med Univ, Brain Res Inst, Shenyang, Peoples R China China Med Univ Shenyang Peoples R China Inst, Shenyang, Peoples R China Zhunyi Med Coll, Dept Pharmacol, Zhunyi, Peoples R China Zhunyi Med Coll Zhunyi Peoples R China armacol, Zhunyi, Peoples R China
Titolo Testata:
JOURNAL OF NEUROTRAUMA
fascicolo: 3, volume: 18, anno: 2001,
pagine: 259 - 273
SICI:
0897-7151(200103)18:3<259:ANMFDB>2.0.ZU;2-N
Fonte:
ISI
Lingua:
ENG
Soggetto:
EXCITATORY AMINO-ACIDS; SPINAL-CORD INJURY; HUMAN HEAD-INJURY; C-JUN EXPRESSION; FOCAL CEREBRAL-ISCHEMIA; CORTICAL IMPACT INJURY; METHYL-D-ASPARTATE; NERVE-CELL DEATH; AXONAL INJURY; RAT-BRAIN;
Keywords:
apoptosis; glutamate; intracranial pressure; microdialysis; taurine; traumatic brain injury;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
75
Recensione:
Indirizzi per estratti:
Indirizzo: Hamberger, A Univ Gothenburg, Dept Anat & Cell Biol, Box 420, SE-40530 Gothenburg, Sweden Univ Gothenburg Box 420 Gothenburg Sweden SE-40530 g, Sweden
Citazione:
M. Runnerstam et al., "A new model for diffuse brain injury by rotational acceleration: II. Effects on extracellular glutamate, intracranial pressure, and neuronal apoptosis", J NEUROTRAU, 18(3), 2001, pp. 259-273

Abstract

The aim of this study is to monitor excitatory amino acids (EAAs) in the extracellular fluids of the brain and to characterize regional neuronal damage in a new experimental model for brain injury, in which rabbits were exposed to 180-260 krad/s(2) rotational head acceleration, This loading causes extensive subarachnoid hemorrhage, focal tissue bleeding, reactive astrocytosis, and axonal damage. Animals were monitored for intracranial pressure (ICP) and for amino acids in the extracellular fluids, Immunohistochemistry was used to study expression of the gene c-Jun and apoptosis with the terminal deoxynucleotidyl transferase nick-end labeling (TUNEL) technique. Extracellular glutamate, glycine, and taurine increased significantly in the hippocampus within a few hours and remained high after 24 h. Neuronal nuclei in the granule layers of the hippocampus and cerebellum were positive for c-Jun after 24 h. Little immunoreactivity was detected in the cerebral cortex. c-Jun-positive neuronal perikarya and processes were found in granule andpyramidal CA4 layers of the hippocampus and among the Purkinje cells of the cerebellum. Also some microglial cells stained positively for c-Jun. TUNEL reactivity was most intense at 10 days after trauma and was extensive in neurons of the cerebral cortex, hippocampus, and cerebellum. The initial response of the brain after rotational head injury involves brain edema after24 h and an excitotoxic neuronal microenvironment in the first hour, whichleads to extensive delayed neuronal cell death by apoptosis necrosis in the cerebral cortex, hippocampus and cerebellum.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 04/06/20 alle ore 01:36:26