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: email@example.com ). 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
AJP - Heart and Circulatory Physiology – The American Physiological Society
Published: Sep 1, 2000
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