Intracellular signal transduction pathways
Cells were treated with the indicated pharmacological inhibitor prior to measuring the rapid and delayed (10 minutes) increase in peak response to NMDA (300 µM) produced by PregS (100 µM). Treatment conditions were as follows: PMA, 10 minutes, 2 µM in Barth’s solution plus 0.5% DMSO; bisindolylmaleimide I, 2–3 hours, 2 µM in Barth’s solution plus 0.5% DMSO; H-89, 1–2 hours, 4 µM in Barth’s solution plus 0.5% DMSO; staurosporine, 2 hours, 2 µM in Barth’s solution plus 0.5% DMSO; DRB, 2 hours, 60 µM in Barth’s solution plus 0.5% DMSO; genistein, 2 hours, 50 µM in Barth’s solution plus 0.5% DMSO; U-0126, 1 hour, 20 µM in Barth’s solution plus 1% DMSO; tyrphostin A47, 20 minutes, 100 µM in Barth’s solution plus 0.5% DMSO.
| Treatment | Target | Total Potentiation | Rapid Potentiation | Delayed Potentiation |
|---|---|---|---|---|
| % | % | % | % | |
| Vehicle | 189 ± 8 | 65 ± 3 | 75 ± 2 (7)a | |
| PMA | PKC | 76 ± 5 | 65 ± 3 | 6 ± 1 (8)* |
| Staurosporine | Protein kinase | 111 ± 7 | 67 ± 2 | 25 ± 3 (8) |
| DRB | Casein kinase | 173 ± 3 | 60 ± 5 | 71 ± 6 (4) |
| Genistein | Nonreceptor protein kinase | 184 ± 6 | 64 ± 4 | 73 ± 3 (5) |
| Vehicle | 199 ± 8 | 66 ± 5 | 81 ± 5 (8) | |
| Bisindolylmaleimide I | PKC | 118 ± 12 | 65 ± 3 | 31 ± 7 (8)** |
| H-89 | PKA | 204 ± 9 | 63 ± 3 | 87 ± 4 (6) |
| Vehicle | 226 ± 18 | 70 ± 4 | 91 ± 6 (8) | |
| U-0126 | MEK | 232 ± 22 | 77 ± 8 | 91 ± 6 (6) |
| Vehicle | 194 ± 19 | 64 ± 8 | 79 ± 8 (6) | |
| Tyrphostin A47 | Insulin receptor Tyr kinase | 210 ± 24 | 72 ± 8 | 80 ± 9 (6) |
DRB, 5,6-dichloro-1-β-d-ribofuranosylbenzimidazole; H-89, N-[2-[[3-(4-bromophenyl)-2-propenyl]amino]ethyl]-5-isoquinolinesulfonamide; MEK, mitogen-activated protein kinase.
↵a The number of oocytes is given in parentheses.
↵* P < 0.01; **P < 0.005 [statistically significant versus vehicle (2-tailed t test)].