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Paul F Worley - One of the best experts on this subject based on the ideXlab platform.
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inhibition of activity dependent arc protein expression in the rat hippocampus impairs the maintenance of long term potentiation and the consolidation of long term memory
The Journal of Neuroscience, 2000Co-Authors: John F. Guzowski, Paul F Worley, James L. Mcgaugh, Gregory L Lyford, Gail D Stevenson, Frank P Houston, Carol A BarnesAbstract:It is widely believed that the brain processes information and stores memories by modifying and stabilizing synaptic connections between neurons. In experimental models of synaptic Plasticity, such as long-term potentiation (LTP), the stabilization of changes in synaptic strength requires rapid de novo RNA and protein synthesis. Candidate genes, which could underlie Activity-Dependent Plasticity, have been identified on the basis of their rapid induction in brain neurons. Immediate-early genes (IEGs) are induced in hippocampal neurons by high-frequency electrical stimulation that induces LTP and by behavioral training that results in long-term memory (LTM) formation. Here, we investigated the role of the IEGArc (also termed Arg3.1) in hippocampal Plasticity. Arc protein is known to be enriched in dendrites of hippocampal neurons where it associates with cytoskeletal proteins (Lyford et al., 1995).Arc is also notable in that its mRNA and protein accumulate in dendrites at sites of recent synaptic activity (Steward et al., 1998). We used intrahippocampal infusions of antisense oligodeoxynucleotides to inhibit Arc protein expression and examined the effect of this treatment on both LTP and spatial learning. Our studies show that disruption of Arc protein expression impairs the maintenance phase of LTP without affecting its induction and impairs consolidation of LTM for spatial water task training without affecting task acquisition or short-term memory. Thus, Arc appears to play a fundamental role in the stabilization of Activity-Dependent hippocampal Plasticity.
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arc a growth factor and activity regulated gene encodes a novel cytoskeleton associated protein that is enriched in neuronal dendrites
Neuron, 1995Co-Authors: Gregory L Lyford, Kanato Yamagata, Laura K Sanders, Walter E. Kaufmann, Carol A Barnes, Neal G Copeland, Debra J Gilbert, Nancy A Jenkins, Anthony Lanahan, Paul F WorleyAbstract:Neuronal activity is an essential stimulus for induction of Plasticity and normal development of the CNS. We have used differential cloning techniques to identify a novel immediate-early gene (IEG) cDNA that is rapidly induced in neurons by activity in models of adult and developmental Plasticity. Both the mRNA and the encoded protein are enriched in neuronal dendrites. Analysis of the deduced amino acid sequence indicates a region of homology with alpha-spectrin, and the full-length protein, prepared by in vitro transcription/translation, coprecipitates with F-actin. Confocal microscopy of the native protein in hippocampal neurons demonstrates that the IEG-encoded protein is enriched in the subplasmalemmal cortex of the cell body and dendrites and thus colocalizes with the actin cytoskeletal matrix. Accordingly, we have termed the gene and encoded protein Arc (activity-regulated cytoskeleton-associated protein). Our observations suggest that Arc may play a role in Activity-Dependent Plasticity of dendrites.
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rheb a growth factor and synaptic activity regulated gene encodes a novel ras related protein
Journal of Biological Chemistry, 1994Co-Authors: Kanato Yamagata, Laura K Sanders, Daniel Nathans, Walter E. Kaufmann, Carol A Barnes, Paul F WorleyAbstract:Abstract Neuronal activity results in long term cellular changes that underlie normal brain development and synaptic Plasticity. To examine the molecular basis of Activity-Dependent Plasticity, we have used differential cloning techniques to identify genes that are rapidly induced in brain neurons by synaptic activity. Here we describe an inducible novel member of the Ras family of small GTP-binding proteins we have termed Rheb. rheb mRNA is rapidly and transiently induced in hippocampal granule cells by seizures and by NMDA-dependent synaptic activity in the long term potentiation paradigm. The predicted amino acid sequence of Rheb is most closely homologous to yeast Ras1 and human Rap2. The putative GTP binding regions are highly conserved. A bacterial fusion protein of Rheb binds GTP and exhibits intrinsic GTPase activity. Like Ha-Ras, the carboxylterminal sequence encodes a CAAX box that is predicted to signal post-translational farnesylation and to target Rheb to specific membranes. rheb mRNA is expressed at comparatively high levels in normal adult cortex as well as a number of peripheral tissues, including lung and intestine. In the developing brain, rheb mRNA is expressed at relatively high levels in embryonic day 19 cortical plate, and expression remains at stable levels throughout the remainder of prenatal and postnatal development. Its close homology with ras and its rapid inducibility by receptor-dependent synaptic activity suggest that rheb may play an important role in long term Activity-Dependent neuronal responses.
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expression of a mitogen inducible cyclooxygenase in brain neurons regulation by synaptic activity and glucocorticoids
Neuron, 1993Co-Authors: Kanato Yamagata, Walter E. Kaufmann, Carol A Barnes, Katrin I Andreasson, Paul F WorleyAbstract:Prostaglandins play important and diverse roles in the CNS. The first step in prostaglandin synthesis involves enzymatic oxidation of arachidonic acid, which is catalyzed by prostaglandin H(PGH) synthase, also referred to as cyclooxygenase. We have cloned an inducible form of this enzyme from rat brain that is nearly identical to a murine, mitogen-inducible cyclooxygenase identified from fibroblasts. Our studies indicate that this gene, here termed COX-2, is expressed throughout the forebrain in discrete populations of neurons and is enriched in the cortex and hippocampus. Neuronal expression is rapidly and transiently induced by seizures or NMDA-dependent synaptic activity. No expression is detected in glia or vascular endothelial cells. Basal expression of COX-2 appears to be regulated by natural synaptic activity in the developing and adult brain. Both basal and induced expression of COX-2 are inhibited by glucocorticoids, consistent with COX-2 regulation in peripheral tissues. Our studies indicate that COX-2 expression may be important in regulating prostaglandin signaling in brain. The marked inducibility in neurons by synaptic stimuli suggests a role in Activity-Dependent Plasticity.
Jonathan R. Wolpaw - One of the best experts on this subject based on the ideXlab platform.
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spinal cord Plasticity in acquisition and maintenance of motor skills
Acta Physiologica, 2007Co-Authors: Jonathan R. WolpawAbstract:Throughout normal life, Activity-Dependent Plasticity occurs in the spinal cord as well as in brain. Like other central nervous system (CNS) Plasticity, spinal cord Plasticity can occur at numerous neuronal and synaptic sites and through a variety of mechanisms. Spinal cord Plasticity is prominent early in life and contributes to mastery of standard behaviours like locomotion and rapid withdrawal from pain. Later in life, spinal cord Plasticity has a role in acquisition and maintenance of new motor skills, and in compensation for peripheral and central changes accompanying ageing, disease and trauma. Mastery of the simplest behaviours is accompanied by complex spinal and supraspinal Plasticity. This complexity is necessary, in order to preserve the complete behavioural repertoire, and is also inevitable, due to the ubiquity of Activity-Dependent CNS Plasticity. Explorations of spinal cord Plasticity are necessary for understanding motor skills. Furthermore, the spinal cord's comparative simplicity and accessibility makes it a logical starting point for studying skill acquisition. Induction and guidance of Activity-Dependent spinal cord Plasticity will probably play an important role in realization of effective new rehabilitation methods for spinal cord injuries, cerebral palsy and other motor disorders.
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operant conditioning of reciprocal inhibition in rat soleus muscle
Journal of Neurophysiology, 2006Co-Authors: Xiang Yang Chen, Lu Chen, Yi Chen, Jonathan R. WolpawAbstract:Operant conditioning of the H-reflex, the electrical analog of the spinal stretch reflex (SSR), induces Activity-Dependent Plasticity in the spinal cord and might be used to improve locomotion afte...
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activity dependent spinal cord Plasticity in health and disease
Annual Review of Neuroscience, 2001Co-Authors: Jonathan R. Wolpaw, Ann M TennissenAbstract:Activity-Dependent Plasticity occurs in the spinal cord throughout life. Driven by input from the periphery and the brain, this Plasticity plays an important role in the acquisition and maintenance of motor skills and in the effects of spinal cord injury and other central nervous system disorders. The responses of the isolated spinal cord to sensory input display sensitization, long-term potentiation, and related phenomena that contribute to chronic pain syndromes; they can also be modified by both classical and operant conditioning protocols. In animals with transected spinal cords and in humans with spinal cord injuries, treadmill training gradually modifies the spinal cord so as to improve performance. These adaptations by the isolated spinal cord are specific to the training regimen and underlie new approaches to restoring function after spinal cord injury. Descending inputs from the brain that occur during normal development, as a result of supraspinal trauma, and during skill acquisition change the spinal cord. The early development of adult spinal cord reflex patterns is driven by descending activity; disorders that disrupt descending activity later in life gradually change spinal cord reflexes. Athletic training, such as that undertaken by ballet dancers, is associated with gradual alterations in spinal reflexes that appear to contribute to skill acquisition. Operant conditioning protocols in animals and humans can produce comparable reflex changes and are associated with functional and structural Plasticity in the spinal cord, including changes in motoneuron firing threshold and axonal conduction velocity, and in synaptic terminals on motoneurons. The corticospinal tract has a key role in producing this Plasticity. Behavioral changes produced by practice or injury reflect the combination of Plasticity at multiple spinal cord and supraspinal sites. Plasticity at multiple sites is both necessary-to insure continued performance of previously acquired behaviors-and inevitable-due to the ubiquity of the capacity for Activity-Dependent Plasticity in the central nervous system. Appropriate induction and guidance of Activity-Dependent Plasticity in the spinal cord is an essential component of new therapeutic approaches aimed at maximizing function after spinal cord injury or restoring function to a newly regenerated spinal cord. Because Plasticity in the spinal cord contributes to skill acquisition and because the spinal cord is relatively simple and accessible, this Plasticity is a logical and practical starting point for studying the acquisition and maintenance of skilled behaviors.
Michael P Stryker - One of the best experts on this subject based on the ideXlab platform.
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autophosphorylation of αcamkii is required for ocular dominance Plasticity
Neuron, 2002Co-Authors: Sharif A Taha, Jessica L Hanover, Alcino J Silva, Michael P StrykerAbstract:Abstract Experience is a powerful sculptor of developing neural connections. In the primary visual cortex (V1), cortical connections are particularly susceptible to the effects of sensory manipulation during a postnatal critical period. At the molecular level, this Activity-Dependent Plasticity requires the transformation of synaptic depolarization into changes in synaptic weight. The molecule α calcium-calmodulin kinase type II (αCaMKII) is known to play a central role in this transformation. Importantly, αCaMKII function is modulated by autophosphorylation, which promotes Ca 2+ -independent kinase activity. Here we show that mice possessing a mutant form of αCaMKII that is unable to autophosphorylate show impairments in ocular dominance Plasticity. These results confirm the importance of αCaMKII in visual cortical Plasticity and suggest that synaptic changes induced by monocular deprivation are stored specifically in glutamatergic synapses made onto excitatory neurons.
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rapid ocular dominance Plasticity requires cortical but not geniculate protein synthesis
Neuron, 2002Co-Authors: Sharif A Taha, Michael P StrykerAbstract:Synaptic Plasticity is a multistep process in which rapid, early phases eventually give way to slower, more enduring stages. Diverse forms of synaptic change share a common requirement for protein synthesis in the late stages of Plasticity, which are often associated with structural rearrangements. Ocular dominance Plasticity in the primary visual cortex (V1) is a long-lasting form of Activity-Dependent Plasticity comprised of well-defined physiological and anatomical stages. The molecular events underlying these stages remain poorly understood. Using the protein synthesis inhibitor cycloheximide, we investigated a role for protein synthesis in ocular dominance Plasticity. Suppression of cortical, but not geniculate, protein synthesis impaired rapid ocular dominance Plasticity, while leaving neuronal responsiveness intact. These findings suggest that structural changes underlying ocular dominance Plasticity occur rapidly following monocular occlusion, and cortical changes guide subsequent alterations in thalamocortical afferents.
Kanato Yamagata - One of the best experts on this subject based on the ideXlab platform.
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arc a growth factor and activity regulated gene encodes a novel cytoskeleton associated protein that is enriched in neuronal dendrites
Neuron, 1995Co-Authors: Gregory L Lyford, Kanato Yamagata, Laura K Sanders, Walter E. Kaufmann, Carol A Barnes, Neal G Copeland, Debra J Gilbert, Nancy A Jenkins, Anthony Lanahan, Paul F WorleyAbstract:Neuronal activity is an essential stimulus for induction of Plasticity and normal development of the CNS. We have used differential cloning techniques to identify a novel immediate-early gene (IEG) cDNA that is rapidly induced in neurons by activity in models of adult and developmental Plasticity. Both the mRNA and the encoded protein are enriched in neuronal dendrites. Analysis of the deduced amino acid sequence indicates a region of homology with alpha-spectrin, and the full-length protein, prepared by in vitro transcription/translation, coprecipitates with F-actin. Confocal microscopy of the native protein in hippocampal neurons demonstrates that the IEG-encoded protein is enriched in the subplasmalemmal cortex of the cell body and dendrites and thus colocalizes with the actin cytoskeletal matrix. Accordingly, we have termed the gene and encoded protein Arc (activity-regulated cytoskeleton-associated protein). Our observations suggest that Arc may play a role in Activity-Dependent Plasticity of dendrites.
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rheb a growth factor and synaptic activity regulated gene encodes a novel ras related protein
Journal of Biological Chemistry, 1994Co-Authors: Kanato Yamagata, Laura K Sanders, Daniel Nathans, Walter E. Kaufmann, Carol A Barnes, Paul F WorleyAbstract:Abstract Neuronal activity results in long term cellular changes that underlie normal brain development and synaptic Plasticity. To examine the molecular basis of Activity-Dependent Plasticity, we have used differential cloning techniques to identify genes that are rapidly induced in brain neurons by synaptic activity. Here we describe an inducible novel member of the Ras family of small GTP-binding proteins we have termed Rheb. rheb mRNA is rapidly and transiently induced in hippocampal granule cells by seizures and by NMDA-dependent synaptic activity in the long term potentiation paradigm. The predicted amino acid sequence of Rheb is most closely homologous to yeast Ras1 and human Rap2. The putative GTP binding regions are highly conserved. A bacterial fusion protein of Rheb binds GTP and exhibits intrinsic GTPase activity. Like Ha-Ras, the carboxylterminal sequence encodes a CAAX box that is predicted to signal post-translational farnesylation and to target Rheb to specific membranes. rheb mRNA is expressed at comparatively high levels in normal adult cortex as well as a number of peripheral tissues, including lung and intestine. In the developing brain, rheb mRNA is expressed at relatively high levels in embryonic day 19 cortical plate, and expression remains at stable levels throughout the remainder of prenatal and postnatal development. Its close homology with ras and its rapid inducibility by receptor-dependent synaptic activity suggest that rheb may play an important role in long term Activity-Dependent neuronal responses.
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expression of a mitogen inducible cyclooxygenase in brain neurons regulation by synaptic activity and glucocorticoids
Neuron, 1993Co-Authors: Kanato Yamagata, Walter E. Kaufmann, Carol A Barnes, Katrin I Andreasson, Paul F WorleyAbstract:Prostaglandins play important and diverse roles in the CNS. The first step in prostaglandin synthesis involves enzymatic oxidation of arachidonic acid, which is catalyzed by prostaglandin H(PGH) synthase, also referred to as cyclooxygenase. We have cloned an inducible form of this enzyme from rat brain that is nearly identical to a murine, mitogen-inducible cyclooxygenase identified from fibroblasts. Our studies indicate that this gene, here termed COX-2, is expressed throughout the forebrain in discrete populations of neurons and is enriched in the cortex and hippocampus. Neuronal expression is rapidly and transiently induced by seizures or NMDA-dependent synaptic activity. No expression is detected in glia or vascular endothelial cells. Basal expression of COX-2 appears to be regulated by natural synaptic activity in the developing and adult brain. Both basal and induced expression of COX-2 are inhibited by glucocorticoids, consistent with COX-2 regulation in peripheral tissues. Our studies indicate that COX-2 expression may be important in regulating prostaglandin signaling in brain. The marked inducibility in neurons by synaptic stimuli suggests a role in Activity-Dependent Plasticity.
Carol A Barnes - One of the best experts on this subject based on the ideXlab platform.
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inhibition of activity dependent arc protein expression in the rat hippocampus impairs the maintenance of long term potentiation and the consolidation of long term memory
The Journal of Neuroscience, 2000Co-Authors: John F. Guzowski, Paul F Worley, James L. Mcgaugh, Gregory L Lyford, Gail D Stevenson, Frank P Houston, Carol A BarnesAbstract:It is widely believed that the brain processes information and stores memories by modifying and stabilizing synaptic connections between neurons. In experimental models of synaptic Plasticity, such as long-term potentiation (LTP), the stabilization of changes in synaptic strength requires rapid de novo RNA and protein synthesis. Candidate genes, which could underlie Activity-Dependent Plasticity, have been identified on the basis of their rapid induction in brain neurons. Immediate-early genes (IEGs) are induced in hippocampal neurons by high-frequency electrical stimulation that induces LTP and by behavioral training that results in long-term memory (LTM) formation. Here, we investigated the role of the IEGArc (also termed Arg3.1) in hippocampal Plasticity. Arc protein is known to be enriched in dendrites of hippocampal neurons where it associates with cytoskeletal proteins (Lyford et al., 1995).Arc is also notable in that its mRNA and protein accumulate in dendrites at sites of recent synaptic activity (Steward et al., 1998). We used intrahippocampal infusions of antisense oligodeoxynucleotides to inhibit Arc protein expression and examined the effect of this treatment on both LTP and spatial learning. Our studies show that disruption of Arc protein expression impairs the maintenance phase of LTP without affecting its induction and impairs consolidation of LTM for spatial water task training without affecting task acquisition or short-term memory. Thus, Arc appears to play a fundamental role in the stabilization of Activity-Dependent hippocampal Plasticity.
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arc a growth factor and activity regulated gene encodes a novel cytoskeleton associated protein that is enriched in neuronal dendrites
Neuron, 1995Co-Authors: Gregory L Lyford, Kanato Yamagata, Laura K Sanders, Walter E. Kaufmann, Carol A Barnes, Neal G Copeland, Debra J Gilbert, Nancy A Jenkins, Anthony Lanahan, Paul F WorleyAbstract:Neuronal activity is an essential stimulus for induction of Plasticity and normal development of the CNS. We have used differential cloning techniques to identify a novel immediate-early gene (IEG) cDNA that is rapidly induced in neurons by activity in models of adult and developmental Plasticity. Both the mRNA and the encoded protein are enriched in neuronal dendrites. Analysis of the deduced amino acid sequence indicates a region of homology with alpha-spectrin, and the full-length protein, prepared by in vitro transcription/translation, coprecipitates with F-actin. Confocal microscopy of the native protein in hippocampal neurons demonstrates that the IEG-encoded protein is enriched in the subplasmalemmal cortex of the cell body and dendrites and thus colocalizes with the actin cytoskeletal matrix. Accordingly, we have termed the gene and encoded protein Arc (activity-regulated cytoskeleton-associated protein). Our observations suggest that Arc may play a role in Activity-Dependent Plasticity of dendrites.
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rheb a growth factor and synaptic activity regulated gene encodes a novel ras related protein
Journal of Biological Chemistry, 1994Co-Authors: Kanato Yamagata, Laura K Sanders, Daniel Nathans, Walter E. Kaufmann, Carol A Barnes, Paul F WorleyAbstract:Abstract Neuronal activity results in long term cellular changes that underlie normal brain development and synaptic Plasticity. To examine the molecular basis of Activity-Dependent Plasticity, we have used differential cloning techniques to identify genes that are rapidly induced in brain neurons by synaptic activity. Here we describe an inducible novel member of the Ras family of small GTP-binding proteins we have termed Rheb. rheb mRNA is rapidly and transiently induced in hippocampal granule cells by seizures and by NMDA-dependent synaptic activity in the long term potentiation paradigm. The predicted amino acid sequence of Rheb is most closely homologous to yeast Ras1 and human Rap2. The putative GTP binding regions are highly conserved. A bacterial fusion protein of Rheb binds GTP and exhibits intrinsic GTPase activity. Like Ha-Ras, the carboxylterminal sequence encodes a CAAX box that is predicted to signal post-translational farnesylation and to target Rheb to specific membranes. rheb mRNA is expressed at comparatively high levels in normal adult cortex as well as a number of peripheral tissues, including lung and intestine. In the developing brain, rheb mRNA is expressed at relatively high levels in embryonic day 19 cortical plate, and expression remains at stable levels throughout the remainder of prenatal and postnatal development. Its close homology with ras and its rapid inducibility by receptor-dependent synaptic activity suggest that rheb may play an important role in long term Activity-Dependent neuronal responses.
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expression of a mitogen inducible cyclooxygenase in brain neurons regulation by synaptic activity and glucocorticoids
Neuron, 1993Co-Authors: Kanato Yamagata, Walter E. Kaufmann, Carol A Barnes, Katrin I Andreasson, Paul F WorleyAbstract:Prostaglandins play important and diverse roles in the CNS. The first step in prostaglandin synthesis involves enzymatic oxidation of arachidonic acid, which is catalyzed by prostaglandin H(PGH) synthase, also referred to as cyclooxygenase. We have cloned an inducible form of this enzyme from rat brain that is nearly identical to a murine, mitogen-inducible cyclooxygenase identified from fibroblasts. Our studies indicate that this gene, here termed COX-2, is expressed throughout the forebrain in discrete populations of neurons and is enriched in the cortex and hippocampus. Neuronal expression is rapidly and transiently induced by seizures or NMDA-dependent synaptic activity. No expression is detected in glia or vascular endothelial cells. Basal expression of COX-2 appears to be regulated by natural synaptic activity in the developing and adult brain. Both basal and induced expression of COX-2 are inhibited by glucocorticoids, consistent with COX-2 regulation in peripheral tissues. Our studies indicate that COX-2 expression may be important in regulating prostaglandin signaling in brain. The marked inducibility in neurons by synaptic stimuli suggests a role in Activity-Dependent Plasticity.
