| | Name | Initial Conc. (uM) | Volume (fL) | Buffered |
| 1 | CaMK-thr306 | 0 | 1.5 | No |
| | This forms due to basal autophosphorylation, but I think it has to be considered as a pathway even if some CaM is floating around. In either case it will tend to block further binding of CaM, and will not display any enzyme activity. See Hanson and Schulman JBC 267:24 pp17216-17224 1992 |
| 2 | CaMKII | 70 | 1.5 | No |
| | Huge conc of CaMKII. In PSD it is 20-40% of protein, so we assume it is around 2.5% of protein in spine as a whole. This level is so high it is unlikely to matter much if we are off a bit. This comes to about 70 uM. |
| 3 | CaMKII*** | 0 | 1.5 | No |
| | From Hanson and Schulman, the CaMKII does a lot of autophosphorylation just after the CaM is released. This prevents further CaM binding and renders the enzyme quite independent of Ca. |
| 4 | CaMKII-CaM | 0 | 1.5 | No |
| 5 | CaMKII-thr286 | 0 | 1.5 | No |
| | I am not sure if we need to endow this one with a lot of enzs. It is likely to be a short-lived intermediate, since it will be phosphorylated further as soon as the CAM falls off. |
| 6 | CaMKII-thr286*-CaM | 0 | 1.5 | No |
| | From Hanson and Schulman, the thr286 is responsible for autonomous activation of CaMKII. |
| 7 | tot_autonomous_CaMKII | 0 | 1.5 | No |
| 8 | tot_CaM_CaMKII | 0 | 1.5 | No |
