The Journal of Neuroscience, January 18, 2006, ():
A Signaling Mechanism from G
q-Protein-Coupled Metabotropic Glutamate Receptors to Gene Expression: Role of the c-Jun N-Terminal Kinase Pathway
J. Neurosci. Yang et al.
26: 971
Supplemental data
Files in this Data Supplement:
- supplemental material
-
Fig. S1. Effects of the Na+ channel blocker TTX on basal and DHPG-induced JNK phosphorylation in cultured rat striatal neurons. TTX (1 μM) incubated 45 min before and during a 10-min treatment with DHPG (100 μM) had no significant effect on the DHPG-stimulated JNK phosphorylation. Representative immunoblots are shown left to the quantified data (mean ± SEM, n = 3-4). *p < 0.05 versus basal levels.
- supplemental material
-
Fig. S2. Effects of the antagonists selective for the NMDA receptor (MK801; A), the AMPA receptor (GYKI52466; B) or the VOCC (nifedipine; C) on basal and DHPG-induced JNK phosphorylation in cultured rat striatal neurons. MK801 (1 μM), GYKI52466 (50 or 100 μM), or nifedipine (20 μM) was incubated 30 min prior to and during a 10-min treatment with NMDA (100 μM), AMPA (100 μM), FPL64176 (20 μM), or DHPG (100 μM). Note that MK801, GYKI52466, and nifedipine blocked the JNK phosphorylation induced by the respective agonist, but not by DHPG. Representative immunoblots are shown above to the quantified data of pJNK1 (mean ± SEM; n = 4-6). *p < 0.05 versus basal levels. +p < 0.05 versus the corresponding agonist alone.
- supplemental material
-
Fig. S3. Effects of the PKC inhibitor on basal and DHPG-induced JNK phosphorylation in cultured rat striatal neurons. Ro-31-8220 (1 μM) was incubated 30 min prior to and during a 10-min treatment with PMA (1 μM) or DHPG (100 μM). Note that Ro-31-8220 blocked the PMA-induced JNK phosphorylation, sparing the DHPG-induced JNK phosphorylation. Representative immunoblots are shown above to the quantified data of pJNK1 (mean ± SEM; n = 4). *p < 0.05 versus basal levels. +p < 0.05 versus PMA alone.
