Integrative Center for Learning and Memory and Brain Research Institute

Los Angeles, CA, United States

Integrative Center for Learning and Memory and Brain Research Institute

Los Angeles, CA, United States
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Kastellakis G.,Foundation for Research and Technology Hellas | Cai D.J.,Integrative Center for Learning and Memory and Brain Research Institute | Mednick S.C.,University of California at Riverside | Silva A.J.,Integrative Center for Learning and Memory and Brain Research Institute | Poirazi P.,Foundation for Research and Technology Hellas
Progress in Neurobiology | Year: 2015

It is generally accepted that complex memories are stored in distributed representations throughout the brain, however the mechanisms underlying these representations are not understood. Here, we review recent findings regarding the subcellular mechanisms implicated in memory formation, which provide evidence for a dendrite-centered theory of memory. Plasticity-related phenomena which affect synaptic properties, such as synaptic tagging and capture, synaptic clustering, branch strength potentiation and spinogenesis provide the foundation for a model of memory storage that relies heavily on processes operating at the dendrite level. The emerging picture suggests that clusters of functionally related synapses may serve as key computational and memory storage units in the brain. We discuss both experimental evidence and theoretical models that support this hypothesis and explore its advantages for neuronal function. © 2015 Elsevier Ltd.


Zhou M.,Integrative Center for Learning and Memory and Brain Research Institute | Li W.,Integrative Center for Learning and Memory and Brain Research Institute | Li W.,Shanghai JiaoTong University | Li W.,Wuxi Mental Health Center | And 20 more authors.
Neuron | Year: 2013

Abnormalities during brain development are thought to cause psychiatric illness and other neurodevelopmental disorders. However, developmental processes such as neurogenesis continue in restricted brain regions of adults, and disruptions of these processes could contribute to the phenotypes of neurodevelopmental disorders. As previously reported, we show that . Disc1 knockdown specifically in adult-born dentate gyrus (DG) neurons results in increased mTOR signaling, hyperexcitability, and neuronal structure deficits. . Disc1 knockdown also resulted in pronounced cognitive and affective deficits, which could be reversed when the affected DG neurons were inactivated. Importantly, reversing increases in mTOR signaling with an FDA-approved inhibitor both prevented and treated these behavioral deficits, even when associated structural deficits were not reversed. Our findings suggest that a component of the affective and cognitive phenotypes in neurodevelopmental disorders may be caused by disruptions in adult-born neurons. Consequently, treatments directed at this cell population may have a significant impact on these phenotypes


PubMed | Integrative Center for Learning and Memory and Brain Research Institute
Type: Journal Article | Journal: Neuron | Year: 2013

Abnormalities during brain development are thought to cause psychiatric illness and other neurodevelopmental disorders. However, developmental processes such as neurogenesis continue in restricted brain regions of adults, and disruptions of these processes could contribute to the phenotypes of neurodevelopmental disorders. As previously reported, we show that Disc1 knockdown specifically in adult-born dentate gyrus (DG) neurons results in increased mTOR signaling, hyperexcitability, and neuronal structure deficits. Disc1 knockdownalso resulted in pronounced cognitive and affective deficits, which could be reversed when the affected DG neurons were inactivated. Importantly, reversing increases in mTOR signaling with an FDA-approved inhibitor both prevented and treated these behavioral deficits, even when associated structural deficits were not reversed. Our findings suggest that a component of the affective and cognitive phenotypes in neurodevelopmental disorders may be caused by disruptions inadult-born neurons. Consequently, treatments directed at this cell population may have a significant impact on these phenotypes.

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