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. Author manuscript; available in PMC: 2009 Aug 28.
Published in final edited form as: Neuron. 2008 Aug 28;59(4):621–633. doi: 10.1016/j.neuron.2008.06.020

Figure 5. Dopamine D1 receptor signaling and cAMP reduces calcium-dependent activation of MEF2 in cultured striatal neurons.

Figure 5

(A) Dopamine D1 receptor stimulation (SKF81297, 10 µM) significantly reduces calcium-dependent activation of MEF2-luciferase activity in cultured striatal neurons (*p<0.05; n=15, five independent experiments, Student's t-test). (B) Forskolin (forsk) treatment (10 µM) of cultured striatal neurons significantly attenuates basal and KCl-induced MRE-luciferase activity. The inset shows the effect of forskolin on basal MRE-luciferase activity over a smaller scale (***p<0.001; n=21, seven independent experiments, Student's t-test). (C) Membrane depolarization (60 mM KCl) of cultured striatal neurons significantly increases CRE-luciferase activity. Treatment with dopamine D1 receptor agonist (SKF81297, 10 µM) significantly increases basal and KCl-induced CREB activity in cultured striatal neurons (***p<0.001; n=9, three independent experiments). (D) Constitutively-active calcineurin (CaNΔCT) blocks the inhibitory effect of forskolin on KCl-induced MEF2 activity (***p<0.001 or N.S. (p>0.05); n=6, two independent experiments, Student's t-test).