The glia-derived protease nexin 1 persists for over 1 year in rat brain areas selectively lesioned by transient global ischaemia.

The re-expression of the developmentally regulated serine protease inhibitor glia-derived nexin (GDN) was investigated 1 year after transient global ischaemia induced by the four-vessel occlusion technique in rats. The CA1 sector of the hippocampus was severely shrunken due to the absence of pyramidal cells, but still clearly discernible due to the continued presence of the parvalbumin-containing GABAergic neurons. In this partially neuron-depleted hippocampus, GDN immunoreactivity was found in reactive astrocytes containing glial fibrillary acidic protein. GDN-positive astrocytes were also found in other lesioned areas, the reticular thalamic nucleus and the cerebellar cortex. Thus, the re-expression of GDN in the adult excitotoxically lesioned brain described previously in the gerbil model of ischaemia persists. The continued presence of the protease inhibitor might disturb the proteolytic balance and lead to the deposition of pathological breakdown products of proteins, e.g. beta-amyloid.