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. Author manuscript; available in PMC: 2014 Feb 1.
Published in final edited form as: J Neurochem. 2012 Dec 26;124(4):558–570. doi: 10.1111/jnc.12102

FIGURE 2.

FIGURE 2

Homocysteine-induced p38 MAPK phosphorylation is dependent on NMDAR mediated Ca2+ influx. (A, C) Neuron cultures were treated with 50 μM L-homocysteine (L-Hcy) for 5 min in the absence or presence of (A) MK810 (5 μM) or APV (200 μM) and (C) EGTA (2 mM). (B, D) Neuron cultures were treated with 50 μM L-Hcy and 30 min after onset of homocysteine treatment (post 30′). (B) NMDA receptor blocker MK810 (5 μM) or APV (200 μM) and (D) EGTA (2 mM) were added, and the incubation was continued for 4 hr. Samples were analyzed using anti-phospho-p38 (upper panel) and p-38 (lower panel) antibodies. The extent of phosphorylation of p38 MAPK was quantified using computer-assisted densitometry and Image J analysis. Values are mean ± s.e.m. (n=3). * Significant difference from 0 min time point (p < 0.001); # significant difference from 5 min or 4 hr homocysteine treatment (p < 0.001).