Table 1.

The effect of an L-type Ca²⁺ channel blocker, ionotropic glutamate receptor antagonists, and GABA receptor antagonists on KCl-depolarization- and L-type Ca²⁺ channel-mediated Ser¹³³ CREB phosphorylation in striatal neurons^a

Antagonist	Treatment
	Antagonist	KCl	Antagonist & KCl	FPL 64176	Antagonist & FPL 64176	n =
nifedipine	1.2±0.23	3.2±0.27	1.4±0.09^*	3.8±0.56	1.2±0.21^*	8
MK 801	0.5±0.11	3.6±0.66	1.4±0.23^*	4.1±0.9	3.5±0.57	8
GYKI 52466	0.8±0.28	3.2±0.33	2.0±0.16^*	3.9±0.39	3.7±0.24	2
DNQX/MK 801	0.4±0.11	2.4±0.18	0.6±0.06^*	3.4±0.36	3.3±0.33	4
Ro 05-3663	1.0±0.10	3.0±0.19	2.1±0.22^*	4.0±0.33	3.6±0.33	6
Ro 05-3663/MK 801	0.4±0.04	3.0±0.19	1.0±0.14^*	4.0±0.33	3.5±0.25	6
bicucullin	1.4±0.06	4.5±0.39	3.1±0.25^*	4.5±0.32	4.0±0.39	2
bicucullin/MK 801	0.8±0.24	4.5±0.39	0.8±0.11^*	4.5±0.32	3.7±0.29	2
picrotoxin	0.9±0.05	4.5±0.39	2.7±0.16^*	4.5±0.32	3.8±0.26	2
picrotoxin/MK 801	0.4±0.14	4.5±0.39	1.1±0.31^*	4.5±0.32	3.5±0.44	2
phaclofen	0.6±0.07	3.0±0.19	1.6±0.19^*	4.0±0.33	3.1±0.25	6
phaclofen/MK 801	0.3±0.05	3.0±0.19	0.7±0.09^*	4.0±0.33	2.3±0.29^*	6

Data are fold induction over untreated control±SEM of imunoblots that were developed with Ser¹³³-phospho-CREB antibody. Control was arbitrarily set to 1. KCL (20 mM)-mediated CREB phosphorylation is blocked by nifedipine (20 μM) and MK 801 (1 μM), and partly blocked by GYKI 52466 (50 μM). FPL 64176 (20 μM)-mediated CREB phsophorylation is not blocked by MK 801. GABA antagonists (Ro 05-3663, 100 μM; bicucullin, 100 μM; picrotoxin, 100 μM; phaclofen 100 μM) partly block CREB phosphorylation after treatment with KCl (see also Figs. 1 and 3).

Asterisks indicate statistical significant differences to treatment with stimulants (Tukey–Kramer HSD). In each experiment, all conditions (e.g. control, antagonist, agonist, antagonist & agonist) were run within one gel and related to each other. Fold-induction is pooled from a number of experiments (see ‘n = ’ at right).