Simultaneous but not independent anisomycin infusions in insular cortex and amygdala hinder stabilization of taste memory when updated

Abstract

Reconsolidation has been described as a process where a consolidated memory returns to a labile state when retrieved. Growing evidence suggests that reconsolidation is, in fact, a destabilization/stabilization process that incorporates updated information to a previously consolidated memory. We used the conditioned taste aversion (CTA) task in order to test this theory. On the first trial, the conditioned stimulus (CS) (saccharin) was associated to the unconditioned stimulus (US) (LiCl injection), and as a result, aversion to saccharin was obtained. The following day, animals were injected with anisomycin in either the insular cortex (IC), central amygdala (CeA), basolateral amygdala (BLA), or simultaneously in IC and CeA or IC and BLA, and a second CTA trial was carried out in which updated information was acquired. Animals were tested 24 h later. When protein synthesis was inhibited in either the IC or CeA, consolidation was affected and previously consolidated memory was unimpaired. However, when both the IC and CeA were simultaneously anisomycin injected, the previously consolidated memory was affected. After repeated association trials, protein synthesis inhibition in the IC and CeA did not have an effect on taste memory. These results suggest that the IC and the CeA are necessary for taste-aversion consolidation, and that both share the previously consolidated memory trace. In addition, our data demonstrated that protein synthesis in either the IC or the CeA suffices to stabilize previously consolidated taste memory when destabilized by incorporation of updated information.

Activation of membrane estrogen receptors attenuates opioid receptor-like1 receptor-mediated antinociception via an ERK-dependent non-genomic mechanism

“…Since mER-induced new gene expression was not expected to occur in the given time frame, a positive anisomycin control could not be employed. Such control is usually employed in studies where known genomic changes are expected to occur (García-DeLaTorre et al 2009; Baumbauer et al 2006; Rosenblum et al, 1993; Flood et al 1973). Moreover, intrathecal anisomycin injection protocol employed in the present study has been previously shown to block peripheral nerve injury-induced accumulation of Shank1 protein in the dorsal horn of lumbar spinal cord in the rat (Miletic et al, 2010).…”

The Role of Reconsolidation and the Dynamic Process of Long-Term Memory Formation and Storage

“…Thus, my interpretation of these and other studies based on multiple learning trials, including attenuation of neophobia, incentive instrumental learning, and the Morris water maze (Hernandez et al, 2002; Rodriguez-Ortiz et al, 2005, 2008; Morris et al, 2006; Rossato et al, 2006; García-DeLaTorre et al, 2009), is twofold. First, in agreement with the authors’ conclusions, during a learning curve, post-trial applications of amnesic treatments disrupt memory retention only when the memory is not in an asymptotic level.…”

Protein degradation and protein synthesis in long-term memory formation

“…Protein synthesis inhibitors infused into the amygdala can impair the reconsolidation of auditory delay fear memories, contextual fear memories, inhibitory avoidance memories, and conditioned taste aversion memories (Nader et al, 2000; Parsons et al, 2006a; Milekic et al, 2007; Jarome et al, 2011, 2012; Rodriguez-Ortiz et al, 2012). Additionally, inhibiting protein synthesis in the hippocampus impairs the reconsolidation of contextual fear memories (Debiec et al, 2002; Lee et al, 2008; Gafford et al, 2011), MWM spatial memories (Artinian et al, 2008), and object recognition memories (Rossato et al, 2007), though it has no effect on inhibitory avoidance memories in the hippocampus (Taubenfeld et al, 2001) or conditioned taste aversion memories in the insular cortex (Garcia-DeLaTorre et al, 2009). These results indicate that new protein synthesis is a necessary step in the transfer of a retrieved memory back to long-term storage, suggesting that both the consolidation and reconsolidation of memories requires de novo protein translation in several brain regions.…”