Novelty exposure overcomes foot shock-induced spatial-memory impairment by processes of synaptic-tagging in rats

• Published in: Proceedings of the National Academy of Sciences - PNAS 2012-01, Vol.109 (3), p.953-958
• Main Authors: Almaguer-Melian, William, Bergado-Rosado, Jorge, Pavón-Fuentes, Nancy, Alberti-Amador, Esteban, Mercerón-Martínez, Daymara, Frey, Julietta U
• Format: Article
• Language: English
• Subjects: Animal cognition; Animal training; Animals; Anisomycin; Behavioral neuroscience; Biological Sciences; Brain; Brain-derived neurotrophic factor; Control groups; Data processing; Electroshock; Exploratory Behavior; Foot; Foot - pathology; Foot shock; Gene Expression Regulation; Hippocampus; Learning; Long term memory; Long term potentiation; Male; Maze Learning; Memory; Memory - physiology; Memory Disorders - physiopathology; Mental stimulation; Novelty; Plasticity (synaptic); Protein Biosynthesis; Protein synthesis; Proteins; Rats; Rats, Wistar; Rodents; Short term memory; Spatial discrimination learning; spatial memory; Stress; Synapses; Synapses - metabolism; Time Factors; Training
• ISSN: 0027-8424; 1091-6490
• DOI: 10.1073/pnas.1114198109

Novelty processing can transform short-term into long-term memory. We propose that this memory-reinforcing effect of novelty could be explained by mechanisms outlined in the "synaptic tagging hypothesis." Initial short-term memory is sustained by a transient plasticity change at activated synapses and sets synaptic tags. These tags are later able to capture and process the plasticity-related proteins (PRPs), which are required to transform a short-term synaptic change into a long-term one. Novelty is involved in inducing the synthesis of PRPs [Moncada D, et al. (2011) Proc Natl Acad Sci USA 108:12937–12936], which are then captured by the tagged synapses, consolidating memory. In contrast to novelty, stress can impair learning, memory, and synaptic plasticity. Here, we address questions as to whether novelty-induced PRPs are able to prevent the loss of memory caused by stress and if the latter would not interact with the tag-setting process. We used water-maze (WM) training as a spatial learning paradigm to test our hypothesis. Stress was induced by a strong foot shock (FS; 5 x 1 mA, 2 s) applied 5 min after WM training. Our data show that FS reduced long-term but not short-term memory in the WM paradigm. This negative effect on memory consolidation was time- and training-dependent. Interestingly, novelty exposure prevented the stress-induced memory loss of the spatial task and increased BDNF and Arc expression. This rescuing effect was blocked by anisomycin, suggesting that WM-tagged synapses were not reset by FS and were thus able to capture the novelty-induced PRPs, re-establishing FS-impaired long-term memory.