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Jennifer A Morton - One of the best experts on this subject based on the ideXlab platform.
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progressive imbalance in the interaction between spatial and procedural memory systems in the r6 2 mouse model of huntington s disease
Neurobiology of Learning and Memory, 2009Co-Authors: Alessandro Ciamei, Jennifer A MortonAbstract:Abstract When Huntington’s disease (HD) patients are tested on cognitive tasks that involve both striatal and hippocampal memory systems, a decline in their striatal function is compensated for by an increase in hippocampal activity that allows these patients to achieve an optimal performance [Voermans, N. C., Petersson, K. M., Daudley, L., Weber, B., van Spaendonck, K. P., Kremer, H. P. H., et al. (2004). Interaction between the human hippocampus and the caudate nucleus during route recognition. Neuron, 43, 427–435]. Our recent study suggests that there is also an imbalance between hippocampal and striatal memory systems in R6/2 mice, a widely used animal model of HD [Ciamei, A., & Morton, A. J. (2008). Rigidity in social and emotional memory in the R6/2 mouse model of Huntington’s disease. Neurobiology of Learning and Memory, 89, 533–544]. However, interactions between multiple memory systems have never been studied directly in HD mice. Here, we used a water maze task to examine striatal and hippocampal systems directly. R6/2 mice were trained to swim from a fixed starting point to a cued platform. During the probe test, the apparatus was rotated by 180°, and mice had to choose between a hidden platform located where the cued platform had been during training (place Learning), and a cued platform that was now located in the opposite quadrant (cue Learning). Probe trial results showed that in 8 week old R6/2 mice the escape response was driven mainly by a cue-based strategy (striatal), whereas by 12 weeks of age, a higher proportion of mice adopted a place-based strategy (hippocampal) to escape from the maze. We conclude that following striatal decline in R6/2 mice between 8 and 12 weeks of age, hippocampal functions emerge to drive the escape response of R6/2 mice.
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progressive imbalance in the interaction between spatial and procedural memory systems in the r6 2 mouse model of huntington s disease
Neurobiology of Learning and Memory, 2009Co-Authors: Alessandro Ciamei, Jennifer A MortonAbstract:When Huntington's disease (HD) patients are tested on cognitive tasks that involve both striatal and hippocampal memory systems, a decline in their striatal function is compensated for by an increase in hippocampal activity that allows these patients to achieve an optimal performance [Voermans, N. C., Petersson, K. M., Daudley, L., Weber, B., van Spaendonck, K. P., Kremer, H. P. H., et al. (2004). Interaction between the human hippocampus and the caudate nucleus during route recognition. Neuron, 43, 427-435]. Our recent study suggests that there is also an imbalance between hippocampal and striatal memory systems in R6/2 mice, a widely used animal model of HD [Ciamei, A., & Morton, A. J. (2008). Rigidity in social and emotional memory in the R6/2 mouse model of Huntington's disease. Neurobiology of Learning and Memory, 89, 533-544]. However, interactions between multiple memory systems have never been studied directly in HD mice. Here, we used a water maze task to examine striatal and hippocampal systems directly. R6/2 mice were trained to swim from a fixed starting point to a cued platform. During the probe test, the apparatus was rotated by 180 degrees, and mice had to choose between a hidden platform located where the cued platform had been during training (place Learning), and a cued platform that was now located in the opposite quadrant (cue Learning). Probe trial results showed that in 8 week old R6/2 mice the escape response was driven mainly by a cue-based strategy (striatal), whereas by 12 weeks of age, a higher proportion of mice adopted a place-based strategy (hippocampal) to escape from the maze. We conclude that following striatal decline in R6/2 mice between 8 and 12 weeks of age, hippocampal functions emerge to drive the escape response of R6/2 mice.
Alessandro Ciamei - One of the best experts on this subject based on the ideXlab platform.
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progressive imbalance in the interaction between spatial and procedural memory systems in the r6 2 mouse model of huntington s disease
Neurobiology of Learning and Memory, 2009Co-Authors: Alessandro Ciamei, Jennifer A MortonAbstract:Abstract When Huntington’s disease (HD) patients are tested on cognitive tasks that involve both striatal and hippocampal memory systems, a decline in their striatal function is compensated for by an increase in hippocampal activity that allows these patients to achieve an optimal performance [Voermans, N. C., Petersson, K. M., Daudley, L., Weber, B., van Spaendonck, K. P., Kremer, H. P. H., et al. (2004). Interaction between the human hippocampus and the caudate nucleus during route recognition. Neuron, 43, 427–435]. Our recent study suggests that there is also an imbalance between hippocampal and striatal memory systems in R6/2 mice, a widely used animal model of HD [Ciamei, A., & Morton, A. J. (2008). Rigidity in social and emotional memory in the R6/2 mouse model of Huntington’s disease. Neurobiology of Learning and Memory, 89, 533–544]. However, interactions between multiple memory systems have never been studied directly in HD mice. Here, we used a water maze task to examine striatal and hippocampal systems directly. R6/2 mice were trained to swim from a fixed starting point to a cued platform. During the probe test, the apparatus was rotated by 180°, and mice had to choose between a hidden platform located where the cued platform had been during training (place Learning), and a cued platform that was now located in the opposite quadrant (cue Learning). Probe trial results showed that in 8 week old R6/2 mice the escape response was driven mainly by a cue-based strategy (striatal), whereas by 12 weeks of age, a higher proportion of mice adopted a place-based strategy (hippocampal) to escape from the maze. We conclude that following striatal decline in R6/2 mice between 8 and 12 weeks of age, hippocampal functions emerge to drive the escape response of R6/2 mice.
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progressive imbalance in the interaction between spatial and procedural memory systems in the r6 2 mouse model of huntington s disease
Neurobiology of Learning and Memory, 2009Co-Authors: Alessandro Ciamei, Jennifer A MortonAbstract:When Huntington's disease (HD) patients are tested on cognitive tasks that involve both striatal and hippocampal memory systems, a decline in their striatal function is compensated for by an increase in hippocampal activity that allows these patients to achieve an optimal performance [Voermans, N. C., Petersson, K. M., Daudley, L., Weber, B., van Spaendonck, K. P., Kremer, H. P. H., et al. (2004). Interaction between the human hippocampus and the caudate nucleus during route recognition. Neuron, 43, 427-435]. Our recent study suggests that there is also an imbalance between hippocampal and striatal memory systems in R6/2 mice, a widely used animal model of HD [Ciamei, A., & Morton, A. J. (2008). Rigidity in social and emotional memory in the R6/2 mouse model of Huntington's disease. Neurobiology of Learning and Memory, 89, 533-544]. However, interactions between multiple memory systems have never been studied directly in HD mice. Here, we used a water maze task to examine striatal and hippocampal systems directly. R6/2 mice were trained to swim from a fixed starting point to a cued platform. During the probe test, the apparatus was rotated by 180 degrees, and mice had to choose between a hidden platform located where the cued platform had been during training (place Learning), and a cued platform that was now located in the opposite quadrant (cue Learning). Probe trial results showed that in 8 week old R6/2 mice the escape response was driven mainly by a cue-based strategy (striatal), whereas by 12 weeks of age, a higher proportion of mice adopted a place-based strategy (hippocampal) to escape from the maze. We conclude that following striatal decline in R6/2 mice between 8 and 12 weeks of age, hippocampal functions emerge to drive the escape response of R6/2 mice.
Federico Bermudezrattoni - One of the best experts on this subject based on the ideXlab platform.
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the forgotten insular cortex its role on recognition memory formation
Neurobiology of Learning and Memory, 2014Co-Authors: Federico BermudezrattoniAbstract:For a long time, the insular cortex (IC) has been related with taste physiology and taste memory processes in animal studies. Recently, the role of the IC has been highlighted by findings involving the IC in non-taste memory formation in both human and animal studies. Recognition memory is based on the ability to assess the familiarity of a previously encountered stimulus, and it is considered a form of declarative memory. In this work, I am proposing that the IC and its related circuitry are highly involved in the conversion of novel to familiar stimulus for both object and taste recognition memory. In addition, I will review some of the molecular mechanisms involved in the modification of novelty to familiarity memory processes, including the role of epigenetic mechanisms on the consolidation of recognition memory within the IC. In the second part of the paper, I will review some of the possible mechanisms to transform a novel taste into a familiar aversive taste by a functional interaction between the IC and the amygdala. In summary, the IC is an important area that will open a new avenue for the study of the mechanisms involved in the Neurobiology of Learning and memory in the near future.
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insular cortex is involved in consolidation of object recognition memory
Learning & Memory, 2005Co-Authors: Federico Bermudezrattoni, Shoki Okuda, Benno Roozendaal, James L McgaughAbstract:Federico Bermudez-Rattoni, Shoki Okuda, Benno Roozendaal, and James L. McGaugh Center for the Neurobiology of Learning and Memory and Department of Neurobiology and Behavior, University of California, Irvine, California 92697-3800, USA; Departamento de Neurociencias, Instituto de Fisiologia Celular, Universidad Nacional Autonoma de Mexico, Mexico D.F., 04510, Mexico; CNS Disorder Research, Tsukuba Research Institute, Banyu Pharmaceutical Co., Tsukuba, Ibaraki, 300-2611, Japan
James L Mcgaugh - One of the best experts on this subject based on the ideXlab platform.
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insular cortex is involved in consolidation of object recognition memory
Learning & Memory, 2005Co-Authors: Federico Bermudezrattoni, Shoki Okuda, Benno Roozendaal, James L McgaughAbstract:Federico Bermudez-Rattoni, Shoki Okuda, Benno Roozendaal, and James L. McGaugh Center for the Neurobiology of Learning and Memory and Department of Neurobiology and Behavior, University of California, Irvine, California 92697-3800, USA; Departamento de Neurociencias, Instituto de Fisiologia Celular, Universidad Nacional Autonoma de Mexico, Mexico D.F., 04510, Mexico; CNS Disorder Research, Tsukuba Research Institute, Banyu Pharmaceutical Co., Tsukuba, Ibaraki, 300-2611, Japan
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the Neurobiology of Learning and memory some reminders to remember
Trends in Neurosciences, 2001Co-Authors: Larry Cahill, James L Mcgaugh, Norman M WeinbergerAbstract:We have learned much about the Neurobiology of Learning and memory in the past 100 years. We have also learned much about how we should, and should not, investigate these complex processes. However, with the rapid recent growth in the field and the influx of investigators not familiar with this past, these crucial lessons too often fail to guide the research of today. Here we highlight some major lessons gleaned from this wealth of experience. These include the need to carefully attend to the Learning/performance distinction, to rely equally on synthetic as well as reductionistic thinking, and to avoid the seduction of simplicity. Examples in which the lessons of history are, and are not, educating current research are also given.
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the brain decade in debate i Neurobiology of Learning and memory
Brazilian Journal of Medical and Biological Research, 2000Co-Authors: Alan D Baddeley, James L Mcgaugh, Larry Cahill, Orlando Francisco Amodeo Bueno, J M Fuster, Ivan Izquierdo, Richard G M Morris, Lynn Nadel, Aryeh Routtenberg, Gilberto Fernando XavierAbstract:This article is a transcription of an electronic symposium in which some active researchers were invited by the Brazilian Society for Neuroscience and Behavior (SBNeC) to discuss the last decade's advances in Neurobiology of Learning and memory. The way different parts of the brain are recruited during the storage of different kinds of memory (e.g., short-term vs long-term memory, declarative vs procedural memory) and even the property of these divisions were discussed. It was pointed out that the brain does not really store memories, but stores traces of information that are later used to create memories, not always expressing a completely veridical picture of the past experienced reality. To perform this process different parts of the brain act as important nodes of the neural network that encode, store and retrieve the information that will be used to create memories. Some of the brain regions are recognizably active during the activation of short-term working memory (e.g., prefrontal cortex), or the storage of information retrieved as long-term explicit memories (e.g., hippocampus and related cortical areas) or the modulation of the storage of memories related to emotional events (e.g., amygdala). This does not mean that there is a separate neural structure completely supporting the storage of each kind of memory but means that these memories critically depend on the functioning of these neural structures. The current view is that there is no sense in talking about hippocampus-based or amygdala-based memory since this implies that there is a one-to-one correspondence. The present question to be solved is how systems interact in memory. The pertinence of attributing a critical role to cellular processes like synaptic tagging and protein kinase A activation to explain the memory storage processes at the cellular level was also discussed.
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conference on the Neurobiology of Learning and memory 4th held in irvine california on 17 20 october 1990
1992Co-Authors: James L Mcgaugh, Norman M Weinberger, Gary Lynch, Larry R SquireAbstract:Abstract : This grant provided partial support for the Fourth Conference on the Neurobiology of Learning and Memory which was held at Irvine, California on October 17-20, 1990. The conference was organized and sponsored by the Center for the Neurobiology of Learning and Memory of the University of California, Irvine. The aim of the conference was to review current fact and theory concerning three research issues in the Neurobiology of Learning and memory: (1) the features and loci of patterns of brain activity induced by Learning, (2) the roles of different brain systems in mediating Learning and memory, and (3) cellular modifications underlying Learning and memory. The presentations and discussions represented all levels of analysis from molecular Neurobiology through systems/behavioral studies. There were 20 principal speakers, 98 poster presentations and over 300 registered participants representing 20 countries. A book based on the proceedings of the conference, Memory: Organization and Locus of Change (Larry R. Squire, Norman M. Weinberger, Gary Lynch and James L. McGaugh, Editors) is in press. Neurobiology of Learning and Memory, Neuroscience, Neuroplasticity.
Manish Vaidya - One of the best experts on this subject based on the ideXlab platform.
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A Neurobiology of Learning beyond the declarative non-declarative distinction
Frontiers in Behavioral Neuroscience, 2013Co-Authors: Daniele Ortu, Manish VaidyaAbstract:In neuroscience and psychology it has become common to distinguish between declarative and non-declarative forms of Learning (e.g., Squire and Zola, 1996). The perspective (Squire, 2004, p. 173) that declarative Learning “refers to the capacity for conscious recollection about facts and events and is the kind of memory that is impaired in amnesia and dependent on structures in the medial temporal lobe” developed when it was observed that patients with hippocampal damage were able to learn and improve on “procedural” tasks, such as hand-eye coordination, without being able to remember the specific Learning episodes (e.g., Scoville and Milner, 1957; Squire, 1992). Such evidence led researchers (e.g., Moscovitch, 1995) to suggest that there are two separate Learning systems: one involved in declarative, conscious, Learning situated in the Medial Temporal Lobe (MTL) comprising the hippocampus, and another involved in non-declarative, implicit, skill/habit Learning involving the basal ganglia. An interpretation of the roles of the hippocampus and the basal ganglia in Learning independent from the declarative/non-declarative dichotomy may allow understanding the role of neural structures critical in Learning without relying on phenomenological categories—difficult to examine from a scientific perspective—such as awareness and consciousness. The very nature of what consciousness is in fact still hotly debated (e.g., Morin, 2006) and grounding an entire taxonomy of Learning and memory on consciousness-based criteria might complicate, instead of simplifying, scientific interpretations, and progress. An alternative perspective to the declarative—non-declarative distinction (e.g., Packard and McGaugh, 1992; McDonald and White, 1993) emphasizes the role of the hippocampus in Learning stimulus-stimulus relations, and of the dorsal striatum in acquiring stimulus-response relations. Such perspective is consistent with a recent review (Henke, 2010) suggesting that neurobiological models of Learning based on consciousness might not be adequate to describe the available experimental evidence.