Figure 5.

IGF1 maintains neuronal viability after stroke. (a) There was no significant difference in the pattern of cortical connections between stroke + saline (n = 5) and stroke + IGF1 (n = 7). (b) There was no significant change in the polar distribution of connections with IGF1 administration compared to stroke + saline (P > 0.05). (c) There was a significant loss of cortical connections between stroke + saline (n = 5) and stroke + JB1 (n = 8). (d) There was a significant decrease in polar distribution of connections with IGF1 blockade (P < 0.001). (e) Photomicrographs of neurons in peri-infarct cortex, showing no change in number across IGF1 treatment conditions. (f) (f) Effects of IGF1 and JB1 on neuronal number in layer 5 in normal control or peri-infarct cortex. IGF1 or JB1 were delivered beginning 7 days after stroke. Stroke (n = 6) induces neuronal cell death in peri-infarct cortex (p < 0.01). This neuronal death is not altered by delivery of IGF1 (n = 5, p > 0.05) or vehicle (n = 5, p > 0.05) into peri-infarct cortex. However, IGF1 blockade with JB1 + hydrogel significantly (n = 5, p < 0.05) increases cell death in peri-infarct cortex when compared to the saline + hydrogel (n = 5) –treated animals post-stroke. (g) Photomicrographs of neurons in peri-infarct cortex, showing decrease in number of neurons with JB1-induced IGF1 signaling blockade. Scale bars, 500 μm (c,g) and 1 mm (a,b,d,e). Note that the location of BDA tracer injection was more lateral in ATRX studies (Fig. 4) than in IGF1/JB1 and Lingo1-Fc/NgR1/NgR2 studies, the latter two of which use the same tracer coordinates; this produces slightly different patterns of intracortical connections. Error bars, s.d, *** p < 0.001 and ** p < 0.01 indicate a significant difference compared to normal control; # < 0.05 indicates a significant difference compared to stroke saline + hydrogel.