(−)- d-Deprenyl attenuates apoptosis in experimental brain ischaemia

(−)- d-Deprenyl protects neurons from oxidative damage and helps to maintain the mitochondrial membrane potential by influencing intracellular anti-apoptotic oncoproteins, such as Bcl-2. The cellular rescue in the penumbra region by (−)- d-deprenyl administration was examined after permanent middle cerebral artery occlusion in rats. (−)- d-Deprenyl was given continuously following permanent middle cerebral artery occlusion. Two days later, the rats were killed and their infarct volumes were determined. Coronal brain sections were stained with terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate deoxyribonucleic acid (DNA) nick-end labelling (TUNEL) and caspase-3, TUNEL and anti-neuronal nuclei (NeuN) double labelling. Neural plasticity was characterized by growth-associated protein-43 (GAP-43) immunohistochemistry. A 1000×1000-μm region was sampled at both cortical margins of the TUNEL-positive area at its borders. The numbers of TUNEL-labelled and TUNEL–caspase-3-labelled cells decreased significantly. (−)- d-Deprenyl treatment increased the number of GAP-43-positive cells. We conclude that (−)- d-deprenyl reduced the number of affected cells and induced neuronal plasticity.