| pubmed-article:19465890 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:19465890 | lifeskim:mentions | umls-concept:C0025260 | lld:lifeskim |
| pubmed-article:19465890 | lifeskim:mentions | umls-concept:C0008810 | lld:lifeskim |
| pubmed-article:19465890 | lifeskim:mentions | umls-concept:C1706470 | lld:lifeskim |
| pubmed-article:19465890 | lifeskim:mentions | umls-concept:C1706469 | lld:lifeskim |
| pubmed-article:19465890 | lifeskim:mentions | umls-concept:C0205352 | lld:lifeskim |
| pubmed-article:19465890 | pubmed:issue | 6 | lld:pubmed |
| pubmed-article:19465890 | pubmed:dateCreated | 2009-6-8 | lld:pubmed |
| pubmed-article:19465890 | pubmed:abstractText | The influence of circadian rhythms on memory has long been studied; however, the molecular prerequisites for their interaction remain elusive. The hippocampus, which is a region of the brain important for long-term memory formation and temporary maintenance, shows circadian rhythmicity in pathways central to the memory-consolidation process. As neuronal plasticity is the translation of numerous inputs, illuminating the direct molecular links between circadian rhythms and memory consolidation remains a daunting task. However, the elucidation of how clock genes contribute to synaptic plasticity could provide such a link. Furthermore, the idea that memory training could actually function as a zeitgeber for hippocampal neurons is worth consideration, based on our knowledge of the entrainment of the circadian clock system. The integration of many inputs in the hippocampus affects memory consolidation at both the cellular and the systems level, leaving the molecular connections between circadian rhythmicity and memory relatively obscure but ripe for investigation. | lld:pubmed |
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| pubmed-article:19465890 | pubmed:language | eng | lld:pubmed |
