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Sleep to Remember
Abstract
Scientists from many disciplines have confirmed and elaborated suspicions that sleep relates somehow to the development of memory. In view of the collective illumination of much congruent data, most neurologists now believe that sleep is integral to learning and memory. At present, the preponderance of behavioral, neuroanatomical, physiological, cellular and molecular evidence supports the idea that periods of sleep cycle actively orchestrate changes in certain categories of memory. If taking long hours of sleep is not always possible, nap can be done rather than consuming caffeine.
Neuroscience becomes more relevant for disciplines pertaining to children's development and education with each passing year. Thus, there is an urgent need for scholars and practitioners in these disciplines to educate themselves about the structure, function, and development of the brain, and to explore the neuroscience literature connected with their areas of professional expertise. A detailed rationale, study strategies, and resources for beginning this process are presented, based on the author's recent experiences. They provide a framework and specific guidelines for those who wish to begin to integrate a neuroscience perspective into their teaching, research, and interactions with the community, and they may arouse the curiosity of those who are not yet interested. Numerous examples of pertinent neuroscience research are included. I wish to express my deep appreciation to William T. Greenough and his colleagues Kathy Bates, Julie Markham, Andrea Beckel-Mitchener, Aaron Grossman, Ivan Jeanne Weiler, James Black, Shawn Kohler, Anna Klintsova, Janice Juraska, and Kara Federmeier for their interest, guidance, and superb conversations about the effect of experience on the brain. I am also grateful to Kent Hutson for assistance in learning about neuroimaging, to Vey M. Nordquist, Joel Lubar, and Gordon Burghardt for information and support, and to Hillary Fouts for suggestions on the writing of the article.
Memory impairment is a common sign of aging. The process of declarative memory (memory of facts and events) requires the hippocampus and involves acquisition, encoding, consolidation, translocation, integration, and retrieval. Encoding and consolidation of memory requires extensive protein synthesis and expression of numerous genes necessary for formation of new synaptic connections and neuronal circuits. The connections are made through dendritic spines (DS), which are new postsynaptic terminals. The most important proteins involved in the formation of DS are PIX, GIT, RAC, PAK, and MLC. The energy for this complex process is provided by GTP. It is proposed that specific peptide "labels" are involved in formation of neuronal circuits for specific memories. Recent studies in our laboratory indicate that peptide SP generated in the rat brain during the formation of memory of dark avoidance is transported by kinesin and binds to KLC3 (light chain of kinesin 3). SP also forms a complex with PIX that triggers the formation of new synapses and provides a specific peptide label for the memory of avoiding dark places. This paper will also discuss the silencing of numerous genes in the brain, which contributes to the decline of memory in Alzheimer's disease and aging. The activity of important silenced genes can be restored by naturally occurring molecules such as curcumin, piperine, and phenylacetylglutamine.
It is accepted that once consolidation is completed memory becomes permanent. However, it has also been suggested that reactivation (retrieval) of the original memory, again, makes it sensitive to the same treatments that affect memory consolidation when given after training. Previous results demonstrated that the immediate post-training intraperitoneal administration of N(omega)-nitro-l-arginine methyl ester (L-NAME), a non-specific inhibitor of nitric oxide synthase (NOS), impairs retention test performance of a one-trial step-through inhibitory avoidance response in adult mice. The effect of L-NAME on retention was attributed to an action on memory consolidation of the original learning. For the first time, we report that the administration of L-NAME after the first retention test (memory reactivation) of the inhibitory avoidance response impairs retention performance over six consecutive days. This impairment effect is dose-and-time dependent and could not be attributed to a retrieval deficit since a mild footshock did not reinstate the original avoidance response and no spontaneous recovery was observed at least 21 days after training. Further support for a storage deficit interpretation as opposed to a retrieval deficit was obtained from the fact that L-NAME's effects after retrieval were not due to state-dependency. The impairment effect of L-NAME was dependent on the age of the original memory. That is, there was an inverse correlation between the susceptibility of the memory trace when reactivated and the time elapsed between training and the first retrieval session. We suggest an action of L-NAME on memory reactivation-induced processes that are different from memory extinction of the original learning extending the biological significance of nitric oxide on memory.
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