Chronic metabolic sequelae of traumatic brain injury: prolonged suppression of somatosensory activation

Chronic metabolic sequelae of traumatic brain injury: prolonged suppression of somatosensory... Abstract Injuries to the brain acutely disrupt normal metabolic function and may deactivate functional circuits. It is unknown whether these metabolic abnormalities improve over time. We used 2-deoxyglucose (2-DG) autoradiographic image-averaging to assess local cerebral glucose utilization (lCMR Glc ) of the rat brain 2 mo after moderate (1.7–2.1 atm) fluid-percussion traumatic brain injury (FPI). Four animal groups ( n = 5 each) were studied: sham-injured rats with and without stimulation of the vibrissae-barrel field ipsilateral to injury; and animals with prior FPI, with or without this stimulation. In sham-injured rats, resting lCMR Glc was normal, and vibrissae stimulation produced right-sided metabolic activation of the ventrolateral thalamic and somatosensory-cortical projection areas. In rats with prior injury, lCMR Glc contralateral to injury was normal, but lCMR Glc of the ipsilateral forebrain was depressed by ∼38–45% compared with shams. Whisker stimulation in rats with prior trauma failed to induce metabolic activation of either cortex or thalamus. Image-mapping of histological material obtained in the same injury model was undertaken to assess the possible influence of injury-induced regional brain atrophy on computed lCMR Glc ; an effect was found only in the lateral cortex at the trauma epicenter. Our results show that, 2 mo after trauma, resting cerebral metabolic perturbations persist, and the whisker-barrel somatosensory circuit shows no signs of functional recovery. deoxyglucose autoradiography trauma barrel circuit vibrissae Footnotes Address for reprint requests and other correspondence: M. D. Ginsberg, Cerebral Vascular Disease Research Center, Dept. of Neurology (D4–5), Univ. of Miami School of Medicine, PO Box 016960, Miami, FL 33101 (E-mail: mdginsberg@stroke.med.miami.edu ). The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked “ advertisement ” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact. Copyright © 2000 the American Physiological Society http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png AJP - Heart and Circulatory Physiology The American Physiological Society

Chronic metabolic sequelae of traumatic brain injury: prolonged suppression of somatosensory activation

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Publisher
The American Physiological Society
Copyright
Copyright © 2011 the American Physiological Society
ISSN
0363-6135
eISSN
1522-1539
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Abstract

Abstract Injuries to the brain acutely disrupt normal metabolic function and may deactivate functional circuits. It is unknown whether these metabolic abnormalities improve over time. We used 2-deoxyglucose (2-DG) autoradiographic image-averaging to assess local cerebral glucose utilization (lCMR Glc ) of the rat brain 2 mo after moderate (1.7–2.1 atm) fluid-percussion traumatic brain injury (FPI). Four animal groups ( n = 5 each) were studied: sham-injured rats with and without stimulation of the vibrissae-barrel field ipsilateral to injury; and animals with prior FPI, with or without this stimulation. In sham-injured rats, resting lCMR Glc was normal, and vibrissae stimulation produced right-sided metabolic activation of the ventrolateral thalamic and somatosensory-cortical projection areas. In rats with prior injury, lCMR Glc contralateral to injury was normal, but lCMR Glc of the ipsilateral forebrain was depressed by ∼38–45% compared with shams. Whisker stimulation in rats with prior trauma failed to induce metabolic activation of either cortex or thalamus. Image-mapping of histological material obtained in the same injury model was undertaken to assess the possible influence of injury-induced regional brain atrophy on computed lCMR Glc ; an effect was found only in the lateral cortex at the trauma epicenter. Our results show that, 2 mo after trauma, resting cerebral metabolic perturbations persist, and the whisker-barrel somatosensory circuit shows no signs of functional recovery. deoxyglucose autoradiography trauma barrel circuit vibrissae Footnotes Address for reprint requests and other correspondence: M. D. Ginsberg, Cerebral Vascular Disease Research Center, Dept. of Neurology (D4–5), Univ. of Miami School of Medicine, PO Box 016960, Miami, FL 33101 (E-mail: mdginsberg@stroke.med.miami.edu ). The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked “ advertisement ” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact. Copyright © 2000 the American Physiological Society

Journal

AJP - Heart and Circulatory PhysiologyThe American Physiological Society

Published: Sep 1, 2000

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