The Effect Of New Protein Synthesis At Prl Cortex

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training. Mice infused with anisomycin (n= 12) immediately after conditioning showed impairment in contextual fear memory compared with vehicle-infused animals (saline, n=18) when tested 24 hours after CFC training (DF=28, F=7.19, t-test: p< 0.05) (Figure 2A). Surprisingly, irrespective of the overall decrease in freezing percentage, mice injected with anisomycin did not show any statistical difference in the level of freezing within the first 2 minutes of the test (Figure 2B). By the third minute of testing, ANI-injected mice show a significant decrease in their level of freezing, showing statistical significant differences until the end of the test (drug × memory minutes of test DF=28, F=13.16, t-test p< 0.01; DF=28, F=7.66, t-test p< 0.01; DF=28, F=5.46, t-test p< 0.05) (Figure 2B). These results suggested that new protein synthesis at PrL cortex is critical for the encoding of contextual fear memories.

To further understand new protein synthesis at PFC, we asked whether other subregions of PFC are also critical for encoding of contextual fear memories. To address this question, we studied the role of cingulate cortex 1 (CG1) region of PFC in encoding. We injected anisomycin to inhibit protein synthesis at CG1. Four separate groups of animals received anisomycin and saline infusions into the adjacent CG1 (Saline, n= 8; ANI, n=6; Figure 2 C and D). As in the case of Prl cortex, anisomicyn was injected shortly after CFC training. Measurements of freezing at 24 hours
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