Here we show that fear memory consolidation requires early post-t

Here we show that fear memory consolidation requires early post-training macromolecular synthesis in the anterior part of the retrosplenial cortex (aRSC), and that reversible pharmacological inactivation of this cortical region impairs recall of recent as well as of remote memories. These results challenge the generally accepted idea that neocortical areas are slow encoding systems that participate in the retrieval of remote memories only.”
“Proteomics were performed using

highly (99.99%) purified cytotrophoblasts from six normal and six pre-eclamptic PLX4032 placentas. Eleven proteins were found which decreased in preeclampsia (actin, glutathione S-transferase, peroxiredoxin 6, aldose reductase, heat shock protein 60 (Hsp60), two molecular forms of heat shock protein 70 (Hsp70) beta-tubulin, subunit

proteasome, ezrin, protein disulfide isomerase, and phosphoglycerate mutase 1). Only one protein, alpha-2-HS-glycoprotein (fetuin), was found to increase its expression. Western blots of actin, Hsp70, ezrin, and glutatione S-transferase confirmed decrease in protein expression. Many of the proteins that decreased are consistent with a state of oxidative stress in the preeclamptic placenta and a decreased cytotrophoblast defense against and response to oxidative stress.”
“Recent research shows that while initial learning is dependent on N-methyl-D-aspartate receptors (NMDArs), relearning can be NMDAr-independent. In the present study Selleck KU55933 we examined whether this switch also occurs following forgetting. The developing animal exhibits much more rapid rates of forgetting than adults, so infant rats were used. It was found that infant rats

required NMDArs to learn fear (Experiment 1), and that this memory was forgotten after 14 d (Experiment 2). Despite forgetting, relearning fear did not require NMDAr activation (Experiment 3), even if it occurred in adulthood (Experiment 5). Importantly, animals only showed NMDAr-independent reacquisition if they had received paired (white noise-shock) training during conditioning and not if they received unpaired presentations of the white noise and shock (Experiment 4). In addition, selleck kinase inhibitor this transition following forgetting was not stimulus specific as learning about a novel stimulus (i.e., light, Experiment 6) was also NMDAr-independent. However, reacquisition to a novel stimulus was NMDAr-dependent if the original fear memory was retained at the time of retraining (Experiment 7). Taken together, these results demonstrate how fear memories acquired early in life can have a long-lasting impact on later learning, even when they have been apparently forgotten (i.e., they are not expressed in the animal’s overt behavior). Further, they support the idea that while memories may be forgotten, they are not gone.”
“The relevance of libraries of annotated MS/MS spectra is growing with the amount of proteomic data generated in high-throughput experiments.

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