Effect of non-selective or selective inhibition of DPIV and DPIV-like proteases on eMCAO-induced neurodegeneration. Nissl-stained brain sections show cortical and striatal infarct areas 7 days post eMCAO, marked with black lines of one (A) vehicle- or (B) IPC1755-treated animal at anterior-posterior level Bregma: 0.40 mm to 0.80 mm. (A) and (B) illustrate infarct areas of individual brain sections corresponding to infarct volumes given in C, columns a and b, respectively. Scale bars = 1 mm (C) Morphometrical analysis of cortical and striatal infarct volumes. Equal volumes (2 μl) of vehicle (column a, e) or IPC1755, a non-selective inhibitor of DPIV/DPIV-like and APN/cAAP protease activity (columns b-d) or the specific DPIV inhibitor sitagliptin (column f) or selective inhibitors of DPII (column g) and DP8/9 (column h) were injected icv (f.c. 10 μM) according to the following time schemes. Columns a, b, e-h: first injection in parallel to eMCAO and subsequently, 6 and 24 h after eMCAO; column c: first injection 2 h after eMCAO and then, 6 and 24 h post eMCAO or column d: first injection 6 h and second injection 24 h after eMCAO. Infarct volumes were analyzed 7 days post eMCAO. Cortical (1) and striatal (2) lesion volumes of ipsilateral rat brain hemispheres were quantified individually. Data are given as relative values (% of control damage of vehicle-treated animals). In general, cortical infarct volumes of vehicle-treated control animals were set to 100% (column a, e). See Results for corresponding absolute infarct sizes (mm3). Data are given as means ± S.E.M., n = 8 - 12 animals per treatment group ***p ≤ 0.001 and *p ≤ 0.05, compared to vehicle-treated animals, t-test.