Abstract
The current dogma suggests that the formation of long-term memory (LTM) is dependent on protein synthesis but persistence of the memory trace is not. However, many of the studies examining the effect of protein synthesis inhibitors (PSIs) on LTM persistence were performed in the hippocampus, which is known to have a time-dependent role in memory storage, rather than the cortex, which is considered to be the main structure to store long-term memories. Here we studied the effect of PSIs on LTM formation and persistence in male Wistar Hola (n⩾5) rats by infusing the protein synthesis inhibitor, anisomycin (100 μg, 1 μl), into the gustatory cortex (GC) during LTM formation and persistence in conditioned taste aversion (CTA). We found that local anisomycin infusion to the GC before memory acquisition impaired LTM formation (P=8.9E−5), but had no effect on LTM persistence when infused 3 days post acquisition (P=0.94). However, when we extended the time interval between treatment with anisomycin and testing from 3 days to 14 days, LTM persistence was enhanced (P=0.01). The enhancement was on the background of stable and non-declining memory, and was not recapitulated by another amnesic agent, APV (10 μg, 1 μl), an N-methyl-D-aspartate receptor antagonist (P=0.54). In conclusion, CTA LTM remains sensitive to the action of PSIs in the GC even 3 days following memory acquisition. This sensitivity is differentially expressed between the formation and persistence of LTM, suggesting that increased cortical protein synthesis promotes LTM formation, whereas decreased protein synthesis promotes LTM persistence.
Highlights
Memory is composed of phases characterized by their sensitivity to molecular and behavioral perturbations, such as protein synthesis inhibitors (PSIs)
We studied the effect of gustatory cortex (GC) cortical protein synthesis inhibition on conditioned taste aversion (CTA) long-term memory (LTM) formation and persistence by stereotactically infusing the protein synthesis inhibitor, anisomycin, into the GC during the different stages of LTM
Testing the animals 3 days later resulted in memory impairment (Figure 4e: n = 8 per group, t15 = 12.6, **P = 0.0001, t test), demonstrating that the sensitivity of LTM to protein synthesis inhibition before memory acquisition applies for weak CTA protocol as well. (c) Anisomycin (n = 9) or vehicle (n = 13) were infused to the gustatory cortex 3 days following weak CTA acquisition
Summary
Memory is composed of phases characterized by their sensitivity to molecular and behavioral perturbations, such as protein synthesis inhibitors (PSIs). Long-term memory (LTM) formation is dependent on transcription and translation processes taking place around the time of memory acquisition.[1,2,3,4] the involvement of protein synthesis in LTM persistence is poorly understood, as a memory trace increases its stability to PSIs as the time interval between memory acquisition and PSI infusion increases.[5,6,7,8]. The gustatory cortex (GC), which resides in the anterior insular cortex, is crucial for learning the association between a taste and potential visceral discomfort or pain This form of associative learning is termed conditioned taste aversion (CTA), and is measured in the lab when a normally appetitive taste (e.g., saccharin) becomes aversive after being paired with gastric distress (e.g., using lithium chloride). We studied the effect of GC cortical protein synthesis inhibition on CTA LTM formation and persistence by stereotactically infusing the protein synthesis inhibitor, anisomycin, into the GC during the different stages of LTM
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