Selective induction of ΔFosB in the brain after transient forebrain ischemia accompanied by an increased expression of galectin-1, and the implication of ΔFosB and galectin-1 in neuroprotection and neurogenesis

Transient forebrain ischemia causes selective induction of ΔFosB, an AP-1 (activator protein-1) subunit, in cells within the ventricle wall or those in the dentate gyrus in the rat brain prior to neurogenesis, followed by induction of nestin, a marker for neuronal precursor cells, or galectin-1, a β-galactoside sugar-binding lectin. The adenovirus-mediated expression of FOSB or ΔFosB induced expression of nestin, glial fibrillary acidic protein and galectin-1 in rat embryonic cortical cells. ΔFosB-expressing cells exhibited a significantly higher survival and proliferation after the withdrawal of B27 supplement than the control or FosB-expressing cells. The decline in the ΔFosB expression in the survivors enhanced the MAP2 expression. The expression of ΔFosB in cells within the ventricle wall of the rat brain also resulted in an elevated expression of nestin. We therefore conclude that ΔFosB can promote the proliferation of quiescent neuronal precursor cells, thus enhancing neurogenesis after transient forebrain ischemia.