Relevance of synaptic tagging and capture to the persistence of long-term potentiation and everyday spatial memory

• Published in: Proceedings of the National Academy of Sciences - PNAS Vol. 107; no. 45; pp. 19537 - 19542
• Main Authors: Wang, Szu-Han, Redondo, Roger L., Morris, Richard G. M., Palmiter, Richard D.
• Format: Journal Article
• Language: English
• Published: United States National Academy of Sciences 09.11.2010; National Acad Sciences
• Subjects: Animals; Behavior, Animal; Behavioral neuroscience; Biological Sciences; Brain; Brain slice preparation; CA1 Region, Hippocampal; Dopamine; Dopamine D1 receptors; Dopamine D5 receptors; Electrophysiological recording; Experimentation; Exploration; Food; Glutamic acid receptors (ionotropic); Hippocampus; Hippocampus - physiology; Long term potentiation; Long-Term Potentiation - physiology; Memory; Memory - physiology; Memory encoding; Memory recall; N-Methyl-D-aspartic acid receptors; Neurobiology; Neurons; Novelty; Physiology; Protein biosynthesis; Protein synthesis; Rats; Receptors; Receptors, Dopamine D1 - physiology; Receptors, Dopamine D5 - physiology; Receptors, N-Methyl-D-Aspartate - physiology; Reinforcement; spatial memory; Synapses; Time Factors
• ISSN: 0027-8424; 1091-6490
• DOI: 10.1073/pnas.1008638107

Memory for inconsequential events fades, unless these happen before or after other novel or surprising events. However, our understanding of the neurobiological mechanisms of novelty-enhanced memory persistence is mainly restricted to aversive or fear-associated memories. We now outline an “everyday appetitive” behavioral model to examine whether and how unrelated novelty facilitates the persistence of spatial memory coupled to parallel electrophysiological studies of the persistence of long-term potentiation (LTP). Across successive days, rats were given one trial per day to find food in different places and later had to recall that day’s location. This task is both hippocampus and NMDA receptor dependent. First, encoding with low reward induced place memory that decayed over 24 h; in parallel, weak tetanization of CA1 synapses in brain slices induced early-LTP fading to baseline. Second, novelty exploration scheduled 30 min after this weak encoding resulted in persistent place memory; similarly, strong tetanization—analogous to novelty—both induced late-LTP and rescued earlyinto late-LTP on an independent but convergent pathway. Third, hippocampal dopamine D1/D5 receptor blockade or protein synthesis inhibition within 15 min of exploration prevented persistent place memory and blocked late-LTP. Fourth, symmetrically, when spatial memory was encoded using strong reward, this memory persisted for 24 h unless encoding occurred under hippocampal D1/D5 receptor blockade. Novelty exploration before this encoding rescued the drug-induced memory impairment. Parallel effects were observed in LTP. These findings can be explained by the synaptic tagging and capture hypothesis.