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Figure 1


Fig. 1. Putative model of actin-regulatory pathways controlled by ionotropic glutamate receptors. Active RhoA interacts with NMDARs at the excitatory PSD and recruits and activates the ROCK/PII complex, thus stabilizing actin. High levels of Ca2+ induce CaMKII-dependent phosphorylation of spinophilin, detaching it from actin and recruiting it to the membrane, where it interacts with Lcf, which in turn activates RhoA. The actin-severing activity of cofilin is controlled by different kinases and phosphatases. LIMK, for example, is a negative-regulator of cofilin activity. Activation of LIMK can occur in a Rac1-dependent manner through its downstream effector PAK. NMDA stimuli could trigger an increase in local Rac1-activity levels through the Rac1-GEFs PIX and Tiam1, consequently increasing the activity of cofilin, which eventually results in higher actin-turnover rates.





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