The Experts below are selected from a list of 81 Experts worldwide ranked by ideXlab platform
Paul R. Benjamin - One of the best experts on this subject based on the ideXlab platform.
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Hungarian Academy of Sciences
2012Co-Authors: Eugeny S. Nikitin, György Kemenes, Dimitris V. Vavoulis, Ildikó Kemenes, Vincenzo Marra, Zsolt Pirger, Maximilian Michel, Jianfeng Feng, Paul R. Benjamin, Sussex Centre For NeuroscienceAbstract:Although synaptic Plasticity is widely regarded as the primary mechanism of memory [1], forms of Nonsynaptic Plasticity, such as increased somal or dendritic excitability or membrane potential depolarization, also have been implicated in learning in both vertebrate and invertebrate experimental systems [2–7]. Compared to synaptic Plasticity, however, there is much less information available on the mechanisms of specific types of Nonsynaptic Plasticity involved in well-defined examples of behavioral memory. Recently, we have shown that learning-induced somal depolarization of an identified modulatory cell type (the cerebral giant cells, CGCs) of the snail Lymnaea stagnalis encodes information that enables the expression of long-term associative memory [8]. The Lymnaea CGCs therefore provide a highly suitable experimental system for investigating th
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Invertebrate Models to Study Learning and Memory: Lymnaea
Encyclopedia of Neuroscience, 2009Co-Authors: Paul R. Benjamin, György KemenesAbstract:The pond snail, Lymnaea, is a key model system for investigating the electrical and molecular basis of associative learning. Both classical and operant conditioning are studied using a variety of conditioned stimuli. One-trial conditioning is possible. Electrical changes have been recorded at a number of neuronal sites in the feeding and respiratory central pattern generator (CPG) circuits that are part of the long-term memory (LTM) trace. These sites include conditioned stimulus (CS) sensory pathways, command, and CPG interneurons and motor neurons. Both synaptic and Nonsynaptic Plasticity (persistent changes in membrane potential) are involved in LTM formation. Molecular mechanisms involve transcriptional regulation of gene expression by CREB and C/EBP and conserved signaling pathways like NO, cGMP, MAPK, and PKA.
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Persistent sodium current is a Nonsynaptic substrate for long-term associative memory.
Current biology : CB, 2008Co-Authors: Eugeny S. Nikitin, Dimitris V. Vavoulis, Ildikó Kemenes, Vincenzo Marra, Zsolt Pirger, Maximilian Michel, Jianfeng Feng, Michael O'shea, Paul R. Benjamin, Gyoergy KemenesAbstract:Although synaptic Plasticity is widely regarded as the primary mechanism of memory [1], forms of Nonsynaptic Plasticity, such as increased somal or dendritic excitability or membrane potential depolarization, also have been implicated in learning in both vertebrate and invertebrate experimental systems [2-7]. Compared to synaptic Plasticity, however, there is much less information available on the mechanisms of specific types of Nonsynaptic Plasticity involved in well-defined examples of behavioral memory. Recently, we have shown that learning-induced somal depolarization of an identified modulatory cell type (the cerebral giant cells, CGCs) of the snail Lymnaea stagnalis encodes information that enables the expression of long-term associative memory [8]. The Lymnaea CGCs therefore provide a highly suitable experimental system for investigating the ionic mechanisms of Nonsynaptic Plasticity that can be linked to behavioral learning. Based on a combined behavioral, electrophysiological, immunohistochemical, and computer simulation approach, here we show that an increase of a persistent sodium current of this neuron underlies its delayed and persistent depolarization after behavioral single-trial classical conditioning. Our findings provide new insights into how learning-induced membrane level changes are translated into a form of long-lasting neuronal Plasticity already known to contribute to maintained adaptive modifications at the network and behavioral level [8].
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Role of Delayed Nonsynaptic Neuronal Plasticity in Long-Term Associative Memory
Current biology : CB, 2006Co-Authors: Ildikó Kemenes, György Kemenes, Eugeny S. Nikitin, Michael O'shea, Volko A. Straub, Kevin Staras, Paul R. BenjaminAbstract:Background It is now well established that persistent Nonsynaptic neuronal Plasticity occurs after learning and, like synaptic Plasticity, it can be the substrate for long-term memory. What still remains unclear, though, is how Nonsynaptic Plasticity contributes to the altered neural network properties on which memory depends. Understanding how Nonsynaptic Plasticity is translated into modified network and behavioral output therefore represents an important objective of current learning and memory research. Results By using behavioral single-trial classical conditioning together with electrophysiological analysis and calcium imaging, we have explored the cellular mechanisms by which experience-induced Nonsynaptic electrical changes in a neuronal soma remote from the synaptic region are translated into synaptic and circuit level effects. We show that after single-trial food-reward conditioning in the snail Lymnaea stagnalis, identified modulatory neurons that are extrinsic to the feeding network become persistently depolarized between 16 and 24 hr after training. This is delayed with respect to early memory formation but concomitant with the establishment and duration of long-term memory. The persistent Nonsynaptic change is extrinsic to and maintained independently of synaptic effects occurring within the network directly responsible for the generation of feeding. Artificial membrane potential manipulation and calcium-imaging experiments suggest a novel mechanism whereby the somal depolarization of an extrinsic neuron recruits command-like intrinsic neurons of the circuit underlying the learned behavior. Conclusions We show that Nonsynaptic Plasticity in an extrinsic modulatory neuron encodes information that enables the expression of long-term associative memory, and we describe how this information can be translated into modified network and behavioral output.
György Kemenes - One of the best experts on this subject based on the ideXlab platform.
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Nonsynaptic Plasticity underlies a compartmentalized increase in synaptic efficacy after classical conditioning
Current biology : CB, 2013Co-Authors: E. S. Nikitin, Pavel M. Balaban, György KemenesAbstract:It is now well documented in both vertebrates and invertebrates that Nonsynaptic as well as synaptic Plasticity can be a substrate for long-term memory [1-4]. Little is known, however, about how learning-induced Nonsynaptic Plasticity can lead to compartmentalized presynaptic changes underlying specific memory traces while leaving other circuit functions of the neuron unaffected. Here, using behavioral, electrophysiological, and optical recording methods, we show that the previously described learning-induced depolarization of a modulatory neuron [5] of the Lymnaea feeding system affects its axonal terminals in a spatially segregated manner. In a side branch of the axon of the cerebral giant cells (CGCs), classical conditioning of intact animals reduced proximal-to-distal attenuation of spike-evoked calcium transients, providing a highly effective mechanism for a compartmentalized increase in synaptic efficacy. Somatic depolarization by current injection, which spreads onto the CGC's axonal side branch [5], and the blocking of A-type potassium channels with 4-aminopyridine had an effect similar to learning on the calcium transients. Both of these experimental manipulations also reduced axonal spike attenuation. These findings suggest that the voltage-dependent inactivation of an A-type potassium current links global Nonsynaptic changes to compartmentalized synaptic changes.
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Molecular and Cellular Mechanisms of Classical Conditioning in the Feeding System of Lymnaea
Invertebrate Learning and Memory, 2013Co-Authors: György KemenesAbstract:Lymnaea provides highly valuable experimental models for top-down analyses of associative learning and memory. Using classical conditioning paradigms, molecular mechanisms of consolidation, maintenance, retrieval, and reconsolidation of associative memory have been investigated. Long-term memory (LTM) forms after multitrial reward and aversive conditioning but, unusually, also after single-trial reward conditioning (“flashbulb memory”). Molecular mechanisms of LTM involve highly conserved signaling pathways (NO/cGMP, cAMP/PKA, MAPK, NMDA receptors, and CaMKII), transcriptional regulation of gene expression by CREB and C/EBP, and new protein synthesis. Cellular mechanisms of LTM involve synaptic or Nonsynaptic Plasticity in key modulatory interneurons of the feeding network. Importantly, a number of molecular processes involved in LTM have been traced from the behavioral level to single identified neurons.
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Hungarian Academy of Sciences
2012Co-Authors: Eugeny S. Nikitin, György Kemenes, Dimitris V. Vavoulis, Ildikó Kemenes, Vincenzo Marra, Zsolt Pirger, Maximilian Michel, Jianfeng Feng, Paul R. Benjamin, Sussex Centre For NeuroscienceAbstract:Although synaptic Plasticity is widely regarded as the primary mechanism of memory [1], forms of Nonsynaptic Plasticity, such as increased somal or dendritic excitability or membrane potential depolarization, also have been implicated in learning in both vertebrate and invertebrate experimental systems [2–7]. Compared to synaptic Plasticity, however, there is much less information available on the mechanisms of specific types of Nonsynaptic Plasticity involved in well-defined examples of behavioral memory. Recently, we have shown that learning-induced somal depolarization of an identified modulatory cell type (the cerebral giant cells, CGCs) of the snail Lymnaea stagnalis encodes information that enables the expression of long-term associative memory [8]. The Lymnaea CGCs therefore provide a highly suitable experimental system for investigating th
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Invertebrate Models to Study Learning and Memory: Lymnaea
Encyclopedia of Neuroscience, 2009Co-Authors: Paul R. Benjamin, György KemenesAbstract:The pond snail, Lymnaea, is a key model system for investigating the electrical and molecular basis of associative learning. Both classical and operant conditioning are studied using a variety of conditioned stimuli. One-trial conditioning is possible. Electrical changes have been recorded at a number of neuronal sites in the feeding and respiratory central pattern generator (CPG) circuits that are part of the long-term memory (LTM) trace. These sites include conditioned stimulus (CS) sensory pathways, command, and CPG interneurons and motor neurons. Both synaptic and Nonsynaptic Plasticity (persistent changes in membrane potential) are involved in LTM formation. Molecular mechanisms involve transcriptional regulation of gene expression by CREB and C/EBP and conserved signaling pathways like NO, cGMP, MAPK, and PKA.
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Role of Delayed Nonsynaptic Neuronal Plasticity in Long-Term Associative Memory
Current biology : CB, 2006Co-Authors: Ildikó Kemenes, György Kemenes, Eugeny S. Nikitin, Michael O'shea, Volko A. Straub, Kevin Staras, Paul R. BenjaminAbstract:Background It is now well established that persistent Nonsynaptic neuronal Plasticity occurs after learning and, like synaptic Plasticity, it can be the substrate for long-term memory. What still remains unclear, though, is how Nonsynaptic Plasticity contributes to the altered neural network properties on which memory depends. Understanding how Nonsynaptic Plasticity is translated into modified network and behavioral output therefore represents an important objective of current learning and memory research. Results By using behavioral single-trial classical conditioning together with electrophysiological analysis and calcium imaging, we have explored the cellular mechanisms by which experience-induced Nonsynaptic electrical changes in a neuronal soma remote from the synaptic region are translated into synaptic and circuit level effects. We show that after single-trial food-reward conditioning in the snail Lymnaea stagnalis, identified modulatory neurons that are extrinsic to the feeding network become persistently depolarized between 16 and 24 hr after training. This is delayed with respect to early memory formation but concomitant with the establishment and duration of long-term memory. The persistent Nonsynaptic change is extrinsic to and maintained independently of synaptic effects occurring within the network directly responsible for the generation of feeding. Artificial membrane potential manipulation and calcium-imaging experiments suggest a novel mechanism whereby the somal depolarization of an extrinsic neuron recruits command-like intrinsic neurons of the circuit underlying the learned behavior. Conclusions We show that Nonsynaptic Plasticity in an extrinsic modulatory neuron encodes information that enables the expression of long-term associative memory, and we describe how this information can be translated into modified network and behavioral output.
Eugeny S. Nikitin - One of the best experts on this subject based on the ideXlab platform.
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Hungarian Academy of Sciences
2012Co-Authors: Eugeny S. Nikitin, György Kemenes, Dimitris V. Vavoulis, Ildikó Kemenes, Vincenzo Marra, Zsolt Pirger, Maximilian Michel, Jianfeng Feng, Paul R. Benjamin, Sussex Centre For NeuroscienceAbstract:Although synaptic Plasticity is widely regarded as the primary mechanism of memory [1], forms of Nonsynaptic Plasticity, such as increased somal or dendritic excitability or membrane potential depolarization, also have been implicated in learning in both vertebrate and invertebrate experimental systems [2–7]. Compared to synaptic Plasticity, however, there is much less information available on the mechanisms of specific types of Nonsynaptic Plasticity involved in well-defined examples of behavioral memory. Recently, we have shown that learning-induced somal depolarization of an identified modulatory cell type (the cerebral giant cells, CGCs) of the snail Lymnaea stagnalis encodes information that enables the expression of long-term associative memory [8]. The Lymnaea CGCs therefore provide a highly suitable experimental system for investigating th
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Persistent sodium current is a Nonsynaptic substrate for long-term associative memory.
Current biology : CB, 2008Co-Authors: Eugeny S. Nikitin, Dimitris V. Vavoulis, Ildikó Kemenes, Vincenzo Marra, Zsolt Pirger, Maximilian Michel, Jianfeng Feng, Michael O'shea, Paul R. Benjamin, Gyoergy KemenesAbstract:Although synaptic Plasticity is widely regarded as the primary mechanism of memory [1], forms of Nonsynaptic Plasticity, such as increased somal or dendritic excitability or membrane potential depolarization, also have been implicated in learning in both vertebrate and invertebrate experimental systems [2-7]. Compared to synaptic Plasticity, however, there is much less information available on the mechanisms of specific types of Nonsynaptic Plasticity involved in well-defined examples of behavioral memory. Recently, we have shown that learning-induced somal depolarization of an identified modulatory cell type (the cerebral giant cells, CGCs) of the snail Lymnaea stagnalis encodes information that enables the expression of long-term associative memory [8]. The Lymnaea CGCs therefore provide a highly suitable experimental system for investigating the ionic mechanisms of Nonsynaptic Plasticity that can be linked to behavioral learning. Based on a combined behavioral, electrophysiological, immunohistochemical, and computer simulation approach, here we show that an increase of a persistent sodium current of this neuron underlies its delayed and persistent depolarization after behavioral single-trial classical conditioning. Our findings provide new insights into how learning-induced membrane level changes are translated into a form of long-lasting neuronal Plasticity already known to contribute to maintained adaptive modifications at the network and behavioral level [8].
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Role of Delayed Nonsynaptic Neuronal Plasticity in Long-Term Associative Memory
Current biology : CB, 2006Co-Authors: Ildikó Kemenes, György Kemenes, Eugeny S. Nikitin, Michael O'shea, Volko A. Straub, Kevin Staras, Paul R. BenjaminAbstract:Background It is now well established that persistent Nonsynaptic neuronal Plasticity occurs after learning and, like synaptic Plasticity, it can be the substrate for long-term memory. What still remains unclear, though, is how Nonsynaptic Plasticity contributes to the altered neural network properties on which memory depends. Understanding how Nonsynaptic Plasticity is translated into modified network and behavioral output therefore represents an important objective of current learning and memory research. Results By using behavioral single-trial classical conditioning together with electrophysiological analysis and calcium imaging, we have explored the cellular mechanisms by which experience-induced Nonsynaptic electrical changes in a neuronal soma remote from the synaptic region are translated into synaptic and circuit level effects. We show that after single-trial food-reward conditioning in the snail Lymnaea stagnalis, identified modulatory neurons that are extrinsic to the feeding network become persistently depolarized between 16 and 24 hr after training. This is delayed with respect to early memory formation but concomitant with the establishment and duration of long-term memory. The persistent Nonsynaptic change is extrinsic to and maintained independently of synaptic effects occurring within the network directly responsible for the generation of feeding. Artificial membrane potential manipulation and calcium-imaging experiments suggest a novel mechanism whereby the somal depolarization of an extrinsic neuron recruits command-like intrinsic neurons of the circuit underlying the learned behavior. Conclusions We show that Nonsynaptic Plasticity in an extrinsic modulatory neuron encodes information that enables the expression of long-term associative memory, and we describe how this information can be translated into modified network and behavioral output.
Ildikó Kemenes - One of the best experts on this subject based on the ideXlab platform.
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Hungarian Academy of Sciences
2012Co-Authors: Eugeny S. Nikitin, György Kemenes, Dimitris V. Vavoulis, Ildikó Kemenes, Vincenzo Marra, Zsolt Pirger, Maximilian Michel, Jianfeng Feng, Paul R. Benjamin, Sussex Centre For NeuroscienceAbstract:Although synaptic Plasticity is widely regarded as the primary mechanism of memory [1], forms of Nonsynaptic Plasticity, such as increased somal or dendritic excitability or membrane potential depolarization, also have been implicated in learning in both vertebrate and invertebrate experimental systems [2–7]. Compared to synaptic Plasticity, however, there is much less information available on the mechanisms of specific types of Nonsynaptic Plasticity involved in well-defined examples of behavioral memory. Recently, we have shown that learning-induced somal depolarization of an identified modulatory cell type (the cerebral giant cells, CGCs) of the snail Lymnaea stagnalis encodes information that enables the expression of long-term associative memory [8]. The Lymnaea CGCs therefore provide a highly suitable experimental system for investigating th
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Persistent sodium current is a Nonsynaptic substrate for long-term associative memory.
Current biology : CB, 2008Co-Authors: Eugeny S. Nikitin, Dimitris V. Vavoulis, Ildikó Kemenes, Vincenzo Marra, Zsolt Pirger, Maximilian Michel, Jianfeng Feng, Michael O'shea, Paul R. Benjamin, Gyoergy KemenesAbstract:Although synaptic Plasticity is widely regarded as the primary mechanism of memory [1], forms of Nonsynaptic Plasticity, such as increased somal or dendritic excitability or membrane potential depolarization, also have been implicated in learning in both vertebrate and invertebrate experimental systems [2-7]. Compared to synaptic Plasticity, however, there is much less information available on the mechanisms of specific types of Nonsynaptic Plasticity involved in well-defined examples of behavioral memory. Recently, we have shown that learning-induced somal depolarization of an identified modulatory cell type (the cerebral giant cells, CGCs) of the snail Lymnaea stagnalis encodes information that enables the expression of long-term associative memory [8]. The Lymnaea CGCs therefore provide a highly suitable experimental system for investigating the ionic mechanisms of Nonsynaptic Plasticity that can be linked to behavioral learning. Based on a combined behavioral, electrophysiological, immunohistochemical, and computer simulation approach, here we show that an increase of a persistent sodium current of this neuron underlies its delayed and persistent depolarization after behavioral single-trial classical conditioning. Our findings provide new insights into how learning-induced membrane level changes are translated into a form of long-lasting neuronal Plasticity already known to contribute to maintained adaptive modifications at the network and behavioral level [8].
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Role of Delayed Nonsynaptic Neuronal Plasticity in Long-Term Associative Memory
Current biology : CB, 2006Co-Authors: Ildikó Kemenes, György Kemenes, Eugeny S. Nikitin, Michael O'shea, Volko A. Straub, Kevin Staras, Paul R. BenjaminAbstract:Background It is now well established that persistent Nonsynaptic neuronal Plasticity occurs after learning and, like synaptic Plasticity, it can be the substrate for long-term memory. What still remains unclear, though, is how Nonsynaptic Plasticity contributes to the altered neural network properties on which memory depends. Understanding how Nonsynaptic Plasticity is translated into modified network and behavioral output therefore represents an important objective of current learning and memory research. Results By using behavioral single-trial classical conditioning together with electrophysiological analysis and calcium imaging, we have explored the cellular mechanisms by which experience-induced Nonsynaptic electrical changes in a neuronal soma remote from the synaptic region are translated into synaptic and circuit level effects. We show that after single-trial food-reward conditioning in the snail Lymnaea stagnalis, identified modulatory neurons that are extrinsic to the feeding network become persistently depolarized between 16 and 24 hr after training. This is delayed with respect to early memory formation but concomitant with the establishment and duration of long-term memory. The persistent Nonsynaptic change is extrinsic to and maintained independently of synaptic effects occurring within the network directly responsible for the generation of feeding. Artificial membrane potential manipulation and calcium-imaging experiments suggest a novel mechanism whereby the somal depolarization of an extrinsic neuron recruits command-like intrinsic neurons of the circuit underlying the learned behavior. Conclusions We show that Nonsynaptic Plasticity in an extrinsic modulatory neuron encodes information that enables the expression of long-term associative memory, and we describe how this information can be translated into modified network and behavioral output.
Gyoergy Kemenes - One of the best experts on this subject based on the ideXlab platform.
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Persistent sodium current is a Nonsynaptic substrate for long-term associative memory.
Current biology : CB, 2008Co-Authors: Eugeny S. Nikitin, Dimitris V. Vavoulis, Ildikó Kemenes, Vincenzo Marra, Zsolt Pirger, Maximilian Michel, Jianfeng Feng, Michael O'shea, Paul R. Benjamin, Gyoergy KemenesAbstract:Although synaptic Plasticity is widely regarded as the primary mechanism of memory [1], forms of Nonsynaptic Plasticity, such as increased somal or dendritic excitability or membrane potential depolarization, also have been implicated in learning in both vertebrate and invertebrate experimental systems [2-7]. Compared to synaptic Plasticity, however, there is much less information available on the mechanisms of specific types of Nonsynaptic Plasticity involved in well-defined examples of behavioral memory. Recently, we have shown that learning-induced somal depolarization of an identified modulatory cell type (the cerebral giant cells, CGCs) of the snail Lymnaea stagnalis encodes information that enables the expression of long-term associative memory [8]. The Lymnaea CGCs therefore provide a highly suitable experimental system for investigating the ionic mechanisms of Nonsynaptic Plasticity that can be linked to behavioral learning. Based on a combined behavioral, electrophysiological, immunohistochemical, and computer simulation approach, here we show that an increase of a persistent sodium current of this neuron underlies its delayed and persistent depolarization after behavioral single-trial classical conditioning. Our findings provide new insights into how learning-induced membrane level changes are translated into a form of long-lasting neuronal Plasticity already known to contribute to maintained adaptive modifications at the network and behavioral level [8].
