Injury to the brain (e.g.,
stroke) results in a disruption of neuronal connectivity and loss of fundamental sensori-motor functions. The subsequent recovery of certain functions involves structural rearrangements in areas adjacent to the
infarct. This remodeling of the injured brain requires trafficking of macromolecular components including
cholesterol and
phospholipids, a transport carried out by
apolipoproteins including
apolipoprotein D (apoD). We investigated the changes in the levels of apoD
mRNA and
protein, and its cellular localization during a recovery period up to 30 days after experimental
stroke in the rat brain. In the core of the
brain infarct, apoD immunoreactivity but not
mRNA increased in dying pyramidal neurons, indicative of cellular redistribution of
lipids. During 2 to 7 days of recovery after
stroke, the apoD levels increased in the peri-
infarct and white matter areas in cells identified as mature oligodendrocytes. The apoD expressing cells were conspicuously located along the rim of the
infarct, suggesting a role for apoD in tissue repair. Furthermore, housing animals in an enriched environment improved sensori-motor function and increased the apoD levels. Our data strongly suggest that apoD is involved in regenerative processes and
scar formation in the peri-
infarct area presumably by enhancing
lipid trafficking.