TEMPORAL AND SPATIAL CHANGES OF QUINOLINIC ACID IMMUNOREACTIVITY IN THE GERBIL HIPPOCAMPUS FOLLOWING TRANSIENT CEREBRAL-ISCHEMIA

Quinolinic acid (QUIN) is an endogenous neurotoxin which originates fr om the kynurenine pathway of tryptophan metabolism. An increase of bra in QUIN level occurs in several degenerative and inflammatory disorder s, but the cellular source of QUIN is still a matter of controversy. I n the present study, the gerbil model of transient global ischemia was used to investigate the time course and the cellular localization of QUIN immunoreactivity. Neurodegeneration was evident in the subiculum and in the CA1 area of the hippocampus 4, 7 and 14 days after ischemia . QUIN positive cells, with microglia-like morphology, appeared in the subiculum and in the CA1, 4 days after ischemia. At 7 days post-ische mia they extended to the whole CA1, disappearing at 14 days. Neither n eurodegeneration nor QUIN positive cells could be detected in ischemic gerbils sacrificed at 1 and 2 days after ischemia and in sham-operate d animals. These findings suggest that microglia-like cells infiltrati ng the degenerating areas of the hippocampus represent the major sourc e of QUIN following transient ischemia in the gerbil. Thus, in situ pr oduction of QUIN in vulnerable brain regions may contribute to the pat hophysiological mechanisms of delayed brain injury. (C) 1998 Elsevier Science B.V. All rights reserved.