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. Author manuscript; available in PMC: 2014 Mar 1.
Published in final edited form as: Synapse. 2012 Dec 8;67(3):145–159. doi: 10.1002/syn.21626

Figure 4.

Figure 4

GP 1a, a selective CB2 receptor agonist, upregulates 5-HT2A receptors via ERK1/2 signaling in CLU213 and A1A1v cells. (A) PD198306, a selective ERK1/2 inhibitor, prevented the effect of GP 1a on 5-HT2A receptor mRNA levels in CLU213 and A1A1v cells. **p<0.01, significant effect of GP 1a treatment on 5-HT2A receptor mRNA levels compared to vehicle treated CLU213 or A1A1v cells. ##p<0.01, significant effect of PD 198306 pretreatment on the GP 1a-induced upregulation of 5-HT2A receptor mRNA in CLU213 cells. (B) PD198306 prevented GP 1a-induced ERK1/2 activation. **p<0.01, significant effect of GP 1a treatment on nuclear pERK levels compared to vehicle control. ##p<0.01, significant effect of GP 1a treatment on nuclear pERK levels compared to the effect of GP 1a treatment in PD198306 pretreated cells. &p<0.05, significant effect of PD198306 pretreatment compared to vehicle controls (C) PD198306 prevented the GP 1a-induced increases in 5-HT2A receptor protein levels in CLU213 cells. *p<0.05, significant effect of GP 1a treatment on 5-HT2A receptor protein levels compared to vehicle treated cells. #p<0.05, significant effect of GP 1a treatment on 5-HT2A receptor protein levels compared to the effect of GP 1a treatment in PD198306 pretreated cells. The data represent mean ± SEM (n=3).