Table 1. Quantitative phenotypes used to constrain and challenge the model.
Name | Treatment | Marker | Value | Ref. | |
non-APA phenotypes | basal | - | cAMP | 60 nM | [23], [121] |
STEPact | 80% | [12] | |||
D32p34 | 0.2–0.5 uM | [122] | |||
D32p75 | 13 uM | [123] | |||
DAsliceD32 | Striatal slices+DA≥10 uM Sampled at 5′. | D32p34 | 12 X basal | [6], [124] | |
D32p75 | 0.5 X basal | ||||
NMDAsliceD32 | Striatal slices+NMDA 100 uM Sampled at 10′. | D32p34 | 0.5 X basal | [40], [125] | |
D32p75 | 0.5 X basal | ||||
activateRAS | 1″ Ca2+ spikes in cult. hipp. cells. | RAS•RAF complex | Hill. h = 4.1 K = 0.8 uM | [49] | |
sensitizedNMDAR | NMDA ± SKF38393 3 uM in cult. MSNs. Sampled at 10′ | ERKpp | Qualitative | [19] | |
trafficNMDAR | PFC slices+DA. t series. | NMDAR currents | Monoexpon.k = 0.15 min−1 | [61] | |
Striatal slices+EtOH. t series. | [60] | ||||
APA-phenotypes | APAib | APA to WT mice. IB. t series | ERKpp | Fig. 4D | [12] |
GluR1p | Fig. 4F | [12], [13] | |||
haploD1R | APA to Drd1a+/− mice. Sampled at 15′. | ERKpp | 0.5 X WT | [19] | |
GluR1p | 1 X WT | ||||
haploGolf | APA to GnaI+/− mice. Sampled at 15′. | ERKpp | 0.9 X WT | [20] | |
GluR1p | 0.6 X WT | ||||
D32KO | APA to D32KO mice. Sampled at 15′. | ERKpp | 0.4 X WT | [12] | |
GluR1p | 0.35 X WT | [13] |
STEPact, non-phosphorylated STEP over total STEP; D32p34, DARPP32 phosphorylated in threonine 34; D32p75, DARPP32 phosphorylated in threonine 75; PFC, prefrontal cortex; APA, acute psychostimulant administration; WT, wild type; IB, immunoblot; ERKpp, active ERK; GluR1p, AMPAR subunit GluR1 phosphorylated in the PKA site; t. series, time series; Monoexp, monoexponential. The names of the phenotypic variables are built from the name and marker columns except for parameterized time series or dose responses where it is used the parameter name instead of the marker.