This property of morphogen signaling could be particularly useful in the context of developing circuits. During development, many circuits undergo activity-dependent synaptic refinement, where plasticity in each circuit is restricted to specific times during development, often referred to as critical periods (Hensch, 2004). Thus, these forms of critical period plasticity occur in a switch-like manner, opening and closing during specific developmental time windows. We speculate that morphogens and their antagonists may provide a biochemical mechanism for spatial and temporal patterning of synaptic plasticity during development. Antiplasticity molecules could also stabilize

circuit function. selleck compound It has long been proposed that mechanisms must exist that oppose correlation based rules for activity-dependent plasticity (e.g., LTP and LTD) (Miller, 1996). These correlation based plasticity rules are thought to confer instability on circuits because repeated potentiation or depression would systematically shift all synapses to higher or lower activities. Homeostatic plasticity (or metaplasticity) has been proposed as a potential solution to this problem (Pratt et al., 2003). We propose that antiplasticity molecules may also perform this stabilizing function. Inappropriate changes in circuit activity could be prevented by expression of molecules such as RIG-3,

whose function is to prevent expression of plasticity. Conversely, mutations Ibrutinib chemical structure in antiplasticity

molecules would perturb circuit activity, and may contribute to cognitive and behavioral disorders. Strains were maintained as described previously at 20°C (Brenner, 1974). OP50 Escherichia coli were used for feeding. The wild-type reference strain was N2 Bristol. Descriptions of allele lesions can be found at www.wormbase.org. The mutant strains used were: eri-1(mg366), lin-15B(n744), rig-3(ok2156), acr-16(ok789), cam-1(ak37), mig-14(ga62), cwn-1(ok546), and egl-20(n585). over RNAi assays were performed in the eri-1; lin-15b background ( Wang et al., 2005). RNAi clones utilized were previously described ( Kamath and Ahringer, 2003 and Kamath et al., 2003). Acute aldicarb assays were performed in triplicate on young adult worms by an experimenter unaware of the identity of the RNAi clone utilized, all as described ( Lackner et al., 1999). Aldicarb (Sigma and Roche) concentration was 1 mM. All quantitative imaging was done using a Olympus PlanAPO 100× 1.4 NA objective and an ORCA100 CCD camera (Hamamatsu). Worms were immobilized with 30 mg/ml BDM (Sigma). Imaging was done in either untreated animals or after a 60 min exposure to 1 mM aldicarb. Line scans of dorsal cord fluorescence were analyzed in Igor Pro (WaveMetrics) using custom-written software (Burbea et al., 2002 and Dittman and Kaplan, 2006).