Table 1.
Neutrophil – macrophage interactions
Brain region |
% of total PMN IR cells colocalized with ED1 |
% of total PMN IR cells not colocalized with ED1 |
||
---|---|---|---|---|
ET-1+water | ET-1+AM-36 | ET-1+water | ET-1+AM-36 | |
Hindlimb cortex | 24±1.7 | 3±2.5*** | 76±1.7 | 97±2.5*** |
Forelimb cortex | 27±0.8 | 16±0.6*** | 73±0.8 | 85±0.9** |
Striatum | 25±0.7 | 11±1.2*** | 75±3.2 | 89±1.3* |
Motor cortex | 31±2.0 | 19±2.2*** | 69±2.0 | 75±4.3 |
Parietal cortex | 29±1.9 | 16±3.3** | 71±2.0 | 84±3.3** |
Barrel cortex | 32±2.0 | 25±2.8* | 68±2.0 | 75±2.8 |
Changes in percentage following AM-36 administration in the number of PMN IR cells colocalized or not colocalized with ED1 in different cerebral regions. AM-36 treatment significantly reduced the total number PMN IR cells that were colocalized with ED1, by approximately 10–15% when compared with vehicle-treated rats. Conversely, the percentage of the total number of PMN IR cells not colocalized with ED1 was increased by approximately 10–15% following AM-36 treatment in all cerebral regions except the motor cortex, where no significant difference existed. Data is presented as mean±s.e.m.
P<0.05
P<0.001
P<0.0001 AM-36 compared with vehicle-treated rats (Kruskal–Wallis ANOVA with Dunn's post-test). n=5–6 in each group.