Effects of injury on the indoleamines in cerebral cortex.
It was shown previously that focal cortical freezing lesions in rats cause widespread depression of local cerebral glucose utilization (LCGU) in cortical areas of the lesioned hemisphere. This was interpreted as reflecting functional depression. The underlying mechanisms were postulated to involve alterations of biogenic amine systems. Accordingly, levels of serotonin (5-HT), its metabolite 5-hydroxyindoleacetic acid (5-HIAA), and its precursor tryptophan were determined by an HPLC method with electrochemical detection in frontoparietal cortical areas of both hemispheres at 4 h and 1, 3, 6, 8, and 10 days after a unilateral cortical freezing lesion. The 5-HT content was significantly lower than normal in the lesioned hemisphere only at 24 h, whereas the 5-HIAA level peaked at 24 h but was significantly elevated above normal values between 4 h and 6 days after lesioning. No changes were noted in 5-HT and 5-HIAA contents in the hemisphere contralateral to the lesion. These results indicate that cortical 5-HT metabolism is increased throughout the lesioned hemisphere of a focally injured brain. The increase in tryptophan content of the lesioned brain appeared to have a time course more closely related to previously demonstrated changes in cortical LCGU than to the increase in 5-HIAA content.
D000818:Animals; D002540:Cerebral Cortex / Q000032:analysis / Q000293:injuries*; D005625:Frontal Lobe / Q000032:analysis; D006897:Hydroxyindoleacetic Acid / Q000032:analysis*; D008297:Male; D010296:Parietal Lobe / Q000032:analysis; D051381:Rats; D011919:Rats, Inbred Strains; D012701:Serotonin / Q000032:analysis*; D014364:Tryptophan / Q000032:analysis
D012701:Serotonin; D006897:Hydroxyindoleacetic Acid; D014364:Tryptophan