Figure 4.

The contribution of the mGluR5-associated signaling pathway to the JNK phosphorylation induced by DHPG in cultured rat striatal neurons. A, Pretreatment of striatal neurons with the PLCβ1 inhibitor U73122 did not reduce the JNK phosphorylation induced by DHPG (n = 4). B, U73122, but not U73343, totally blocked the increases in PI hydrolysis induced by DHPG (n = 3–5). U73122 or U73343 at 40μm was incubated 30 min before DHPG (100μm) for 10 min (A) or 0.5–1 min (B). C, Thapsigargin (Thap) did not reduce the JNK phosphorylation induced by DHPG (n = 4). D, The Ca²⁺ chelator BAPTA-AM had no effect on JNK phosphorylation (n = 5). E, DHPG (100μm; 10 min) induced a comparable increase in JNK phosphorylation in either Ca²⁺-containing or Ca²⁺-free medium (n = 4–5). F, Thapsigargin and BAPTA-AM completely blocked intracellular Ca²⁺ rises induced by DHPG (100 μm). In C, D, and F, thapsigargin (2 μm) or BAPTA-AM (30 μm) was incubated 1 h before and during a 10 min treatment with DHPG (100μm). Values in F are expressed as mean-fold changes of basal levels in terms of the peak amplitude of Ca²⁺ responses measured within 1 min after the start of DHPG treatment from 16 to 24 neurons. *p < 0.05 versus basal levels. ⁺p < 0.05 versus DHPG (100μm) alone.