Table 2.
No difference in mGluR-stimulated MAPK or PI3K activation in the Fmr1 KO
| Protein | Phosphorylation site | Phospho/total |
Animals | |||
|---|---|---|---|---|---|---|
| WT | WT + DHPG | KO | KO + DHPG | |||
| Erk1/2* | Thr202/Tyr204 | 100 ± 6% | 132 ± 8% | 90 ± 6% | 135 ± 6% | 13 |
| Akt | Ser473 | 100 ± 5% | 104 ± 6% | 100 ± 5% | 100 ± 6% | 14 |
| p38 | Thr180/Tyr182 | 100 ± 5% | 112 ± 9% | 84 ± 5% | 94 ± 7% | 9 |
| PTEN | Ser380/Thr382/383 | 100 ± 10% | 91 ± 11% | 80 ± 11% | 94 ± 12% | 7 |
| mTOR | Ser2448 | 100 ± 11% | 105 ± 8% | 117 ± 12% | 102 ± 5% | 12 |
| p70S6K | Thr389 | 100 ± 7% | 105 ± 3% | 119 ± 7% | 100 ± 9% | 8 |
| S6 | Ser235/236 | 100 ± 10% | 97 ± 9% | 85 ± 10% | 83 ± 3% | 6 |
Hippocampal slices were stimulated with 100 μm DHPG or vehicle for exactly 5 min. Activation states of ERK1/2, p38, and the PI3K pathway proteins PTEN, Akt, mTOR, p70S6K, and S6 were measured in Fmr1 KO and WT. Results are expressed as % average WT control ± SEM Of the proteins examined, only ERK1/2 was activated by Gp 1 mGluR stimulation (ANOVA treatment, p < 0.0001, genotype x treatment, p = 0.07). This increase was seen in both WT (t test *p < 0.0001) and Fmr1 KO (t test, *p < 0.0001). A small but significant decrease in the activation state of p38 was also observed in Fmr1 KO (t test, *p < 0.05). For each animal, 1–2 slices were analyzed. Data from untreated slices are incorporated in the dataset shown in Table 1; ERK1/2 and Akt data are graphically represented in Figure 2. ANOVA treatment, *p < 0.0001.