TABLE 2.

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.

^aThe number of oocytes is given in parentheses.

^*P < 0.01; **P < 0.005 [statistically significant versus vehicle (2-tailed t test)].