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. Author manuscript; available in PMC: 2011 Dec 22.
Published in final edited form as: Neuron. 2010 Dec 22;68(6):1143–1158. doi: 10.1016/j.neuron.2010.11.034

Figure 8. Parallel roles for dendritic protein synthesis in compensatory presynaptic and postsynaptic changes induced by AMPAR blockade.

Figure 8

Model depicting key events underlying rapid homeostatic compensation. AMPAR blockade induces rapid postsynaptic compensation via synaptic incorporation of GluA1 homomeric AMPARs (Thiagarajan et al., 2005) that emerges rapidly (< 3 hrs) and requires new protein synthesis. Studies examining the effects of NMDAR mini blockade have shown that the compensatory synaptic incorporation of GluA1 homomers requires local dendritic synthesis, likely of GluA1 itself (Ju et al., 2004; Sutton et al., 2006; Aoto et al., 2008). These changes in GluA1 are observed equally in the presence and absence of spiking activity (Figure 1). In parallel, AMPAR blockade induces rapid presynaptic compensation that requires coincident activity in presynaptic terminals. The presynaptic changes require the synthesis and release of BDNF, which is locally translated in dendrites in response to AMPAR blockade.