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  • 1
    Publication Date: 2007-04-21
    Description: Competition between neurons is necessary for refining neural circuits during development and may be important for selecting the neurons that participate in encoding memories in the adult brain. To examine neuronal competition during memory formation, we conducted experiments with mice in which we manipulated the function of CREB (adenosine 3',5'-monophosphate response element-binding protein) in subsets of neurons. Changes in CREB function influenced the probability that individual lateral amygdala neurons were recruited into a fear memory trace. Our results suggest a competitive model underlying memory formation, in which eligible neurons are selected to participate in amemorytrace as a function of their relative CREB activity at the time of learning.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Han, Jin-Hee -- Kushner, Steven A -- Yiu, Adelaide P -- Cole, Christy J -- Matynia, Anna -- Brown, Robert A -- Neve, Rachael L -- Guzowski, John F -- Silva, Alcino J -- Josselyn, Sheena A -- AG13622/AG/NIA NIH HHS/ -- P01HD33098/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 2007 Apr 20;316(5823):457-60.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Program in Neurosciences and Mental Health, Hospital for Sick Children, 555 University Avenue, Toronto, Ontario M5G 1X8, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17446403" target="_blank"〉PubMed〈/a〉
    Keywords: Amygdala/*physiology ; Animals ; Conditioning (Psychology) ; Cyclic AMP Response Element-Binding Protein/genetics/*metabolism ; Cytoskeletal Proteins/genetics/metabolism ; Fear ; Genetic Vectors ; Memory/*physiology ; Mice ; Nerve Tissue Proteins/genetics/metabolism ; Neuronal Plasticity ; Neurons/metabolism/*physiology ; Transcription, Genetic
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
    Publication Date: 2009-03-17
    Description: Memories are thought to be encoded by sparsely distributed groups of neurons. However, identifying the precise neurons supporting a given memory (the memory trace) has been a long-standing challenge. We have shown previously that lateral amygdala (LA) neurons with increased cyclic adenosine monophosphate response element-binding protein (CREB) are preferentially activated by fear memory expression, which suggests that they are selectively recruited into the memory trace. We used an inducible diphtheria-toxin strategy to specifically ablate these neurons. Selectively deleting neurons overexpressing CREB (but not a similar portion of random LA neurons) after learning blocked expression of that fear memory. The resulting memory loss was robust and persistent, which suggests that the memory was permanently erased. These results establish a causal link between a specific neuronal subpopulation and memory expression, thereby identifying critical neurons within the memory trace.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Han, Jin-Hee -- Kushner, Steven A -- Yiu, Adelaide P -- Hsiang, Hwa-Lin Liz -- Buch, Thorsten -- Waisman, Ari -- Bontempi, Bruno -- Neve, Rachael L -- Frankland, Paul W -- Josselyn, Sheena A -- New York, N.Y. -- Science. 2009 Mar 13;323(5920):1492-6. doi: 10.1126/science.1164139.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Program in Neurosciences and Mental Health, Hospital for Sick Children, 555 University Avenue, Toronto, ON, M5G 1X8, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19286560" target="_blank"〉PubMed〈/a〉
    Keywords: Amnesia/*physiopathology ; Amygdala/cytology/*physiology ; Animals ; Apoptosis ; Conditioning (Psychology) ; Cyclic AMP Response Element-Binding Protein/genetics/metabolism ; *Fear ; Memory/*physiology ; Mental Recall/*physiology ; Mice ; Mice, Transgenic
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
    Publication Date: 2014-05-09
    Description: Throughout life, new neurons are continuously added to the dentate gyrus. As this continuous addition remodels hippocampal circuits, computational models predict that neurogenesis leads to degradation or forgetting of established memories. Consistent with this, increasing neurogenesis after the formation of a memory was sufficient to induce forgetting in adult mice. By contrast, during infancy, when hippocampal neurogenesis levels are high and freshly generated memories tend to be rapidly forgotten (infantile amnesia), decreasing neurogenesis after memory formation mitigated forgetting. In precocial species, including guinea pigs and degus, most granule cells are generated prenatally. Consistent with reduced levels of postnatal hippocampal neurogenesis, infant guinea pigs and degus did not exhibit forgetting. However, increasing neurogenesis after memory formation induced infantile amnesia in these species.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Akers, Katherine G -- Martinez-Canabal, Alonso -- Restivo, Leonardo -- Yiu, Adelaide P -- De Cristofaro, Antonietta -- Hsiang, Hwa-Lin Liz -- Wheeler, Anne L -- Guskjolen, Axel -- Niibori, Yosuke -- Shoji, Hirotaka -- Ohira, Koji -- Richards, Blake A -- Miyakawa, Tsuyoshi -- Josselyn, Sheena A -- Frankland, Paul W -- MOP74650/Canadian Institutes of Health Research/Canada -- MOP86762/Canadian Institutes of Health Research/Canada -- New York, N.Y. -- Science. 2014 May 9;344(6184):598-602. doi: 10.1126/science.1248903.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Program in Neurosciences and Mental Health, The Hospital for Sick Children, Toronto, M5G 1X8, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24812394" target="_blank"〉PubMed〈/a〉
    Keywords: Amnesia/*pathology/*physiopathology ; Animals ; Dentate Gyrus/cytology ; Female ; Guinea Pigs ; Hippocampus/*cytology ; Male ; *Memory ; Mice ; Mice, Inbred C57BL ; *Neurogenesis ; Neurons/cytology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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