SYNTHESIS OF SEROTONIN IN TRAUMATIZED RAT-BRAIN

Previous studies have demonstrated that focal freezing lesions in rats cause a widespread decrease of cortical glucose use in the lesioned h emisphere and this was interpreted as a reflection of depression of co rtical activity. The serotonergic neurotransmitter system was implicat ed in these alterations when it was shown that (1) cortical serotonin metabolism was increased widely in focally injured brain and (2) inhib ition of serotonin synthesis prevented the development of cortical hyp ometabolism. In the present studies we applied an autoradiographic met hod that uses the accumulation of the C-14- labeled analogue of seroto nin alpha-methylserotonin to assess changes in the rate of serotonin s ynthesis in injured brain. The results confirmed that 3 days after the lesion was made, at the time of greatest depression of glucose use, s erotonin synthesis was significantly increased in cortical areas throu ghout the injured hemisphere. The increase was also seen in the dorsal hippocampus and area CA3, as well as in the medial geniculate and dor sal raphe, but not in any other subcortical structures including media n raphe. Present results suggest that the functional changes in the co rtex of the lesioned hemisphere are associated with an increased rate of serotonin synthesis mediated by activation of the dorsal raphe. We also documented by alpha-[C-14] aminoisobutyric acid autoradiography t hat there was increased permeability of the blood-brain barrier, but t his was restricted to the rim of the lesion.