Effects of a traumatic neocortical lesion on cerebral metabolism and gene expression of rats.
The effects of a traumatic neocortical lesions, induced by transcranial cold injury, on brain metabolism and gene expression were examined. The surrounding of the lesions was characterized by increased glucose and lactate levels without major disturbances of protein synthesis or energy state. A transient pH decrease by 0.4 units was noticed 1 h post-injury, which shifted towards alkaline values by 3 h. The metabolic disturbances did not differ between injured animals with spontaneous spreading depressions (SD, n = 14) and those without SD (n = 7). In SD animals, c-fos mRNA was strongly elevated in the injury-remote cortex, but hsp72 mRNA was not enhanced. Thus, in contrast to focal ischemia, the metabolic dysfunction around traumatic cortical lesions is not aggravated by SD.
Hermann
D M
DM
Max-Planck-Institute for Neurological Research, Department of Experimental Neurology, Cologne, Germany.
Mies
G
G
Hossmann
K A
KA
D000255:Adenosine Triphosphate / Q000378:metabolism; D000704:Analysis of Variance; D000818:Animals; D001921:Brain / Q000378:metabolism*; D004569:Electroencephalography; D005786:Gene Expression Regulation / Q000502:physiology*; D005947:Glucose / Q000378:metabolism; D050884:HSP72 Heat-Shock Proteins; D006360:Heat-Shock Proteins / Q000235:genetics; D006863:Hydrogen-Ion Concentration; D017403:In Situ Hybridization; D019344:Lactic Acid / Q000378:metabolism; D017078:Laser-Doppler Flowmetry; D008297:Male; D019579:Neocortex / Q000293:injuries / Q000378:metabolism*; D009419:Nerve Tissue Proteins / Q000096:biosynthesis; D051381:Rats; D017207:Rats, Sprague-Dawley
D050884:HSP72 Heat-Shock Proteins; D006360:Heat-Shock Proteins; D009419:Nerve Tissue Proteins; D019344:Lactic Acid; D000255:Adenosine Triphosphate; D005947:Glucose