The Experts below are selected from a list of 309 Experts worldwide ranked by ideXlab platform
Marina A Lynch - One of the best experts on this subject based on the ideXlab platform.
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Long Term Potentiation and memory
Physical Review, 2004Co-Authors: Marina A LynchAbstract:Lynch, MA. Long-Term Potentiation and Memory. Physiol Rev 84: 87–136, 2004; 10.1152/physrev.00014.2003.—One of the most significant challenges in neuroscience is to identify the cellular and molecu...
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Long-Term Potentiation in the dentate gyrus: induction and increased glutamate release are blocked by D(-)aminophosphonovalerate.
Neuroscience, 2003Co-Authors: M.l. Errington, Marina A Lynch, Tim V. P. BlissAbstract:Abstract d (−)Aminophosphonovalerate, a specific antagonist of the N-methyl- d -aspartate subtype of glutamate receptor, was perfused through a push-pull cannula into the dentate gyrus of rats anaesthetized with urethan in order to observe its effect on the induction and maintenance of Long-Term Potentiation and on the increase in release of endogenous glutamate associated with Long-Term Potentiation. The amplitude of the population spike evoked by single test shocks to the perforant path was significantly depressed by 100 μM d (−)aminophosphonovalerate, but there was a minimal effect on the slope of the population excitatory postsynaptic potential, or on the concentration of glutamate released into the perfusate. A brief high-intensity tetanus given to the perforant path while d (−)aminophosphonovalerate was being perfused failed to induce Long-Term Potentiation or the sustained increase in glutamate release associated with Long-Term Potentiation. Short-Term post-tetanic Potentiation was not affected. After wash-out of d (−)aminophosphonovalerate, a second high-frequency train produced both Long-Term Potentiation and an increase in glutamate release which was sustained for the subsequent l h period of observation. d (−)Aminophosphonovalerate did not suppress Long-Term Potentiation once it had been induced. d (−)Aminophosphonovalerate (100 μM) did not itself affect in vivo release of glutamate. However, in a separate series of in vitro experiments, d (−)aminophosphonovalerate at concentrations of 50 μ M and above was found to depress the Ca 2+ -dependent, K + -stimulated release of preloaded [ 14 C]-glutamate from dentate slices. These results suggest that in the dentate gyrus activation of the N-methyl- d -aspartate receptor is required for the induction though not the maintenance of Long-Term Potentiation. The possibility that presynaptic mechanisms contribute to the suppression of Long-Term Potentiation should not be overlooked in view of our in vitro data. The further demonstration in these experiments that a high-frequency train produces a sustained increase in glutamate release only when it also produces Long-Term Potentiation provides additional evidence for the view that the maintenance of Long-Term Potentiation is due, at least in part, to a presynaptic mechanism.
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Evidence for a role for synaptophysin in expression of Long-Term Potentiation in rat dentate gyrus.
Neuroreport, 1998Co-Authors: Patricia M. Mullany, Marina A LynchAbstract:: Maintenance of Long-Term Potentiation in perforant path-granule cell synapses is accompanied by increased glutamate release. Here we investigate the role of synaptophysin in release and in expression of Long-Term Potentiation in dentate gyrus. We report that Long-Term Potentiation was accompanied by increased endogenous glutamate release and increased tyrosine phosphorylation of synaptophysin, but these changes were attenuated when Long-Term Potentiation was inhibited by the tyrosine kinase inhibitor tyrphostin AG879 or by the NMDA antagonist D-aminophosphonovalerate. In vitro analysis revealed that KCl-induced glutamate release was abolished in synaptosomes prepared in the presence of antisynaptophysin. The data suggest a role for synaptophysin in release and indicate that activation of tyrosine kinase and synaptophysin phosphorylation contribute to Long-Term Potentiation perhaps by modulating glutamate release.
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Increase in synaptic vesicle proteins accompanies Long-Term Potentiation in the dentate gyrus
Neuroscience, 1994Co-Authors: Marina A Lynch, K. L. Voss, J. Rodriguez, Tim V. P. BlissAbstract:Maintenance of Long-Term Potentiation in synapses formed by the perforant path on to granule cells of the dentate gyrus is accompanied by a sustained increase in the extracellular concentration of glutamate,3,4 the presumed transmitter at this excitatory hippocampal pathway. Quantal analysis2,12,13,19,27 indicates that, at least in the first hour of induction, this reflects an increase in transmitter release rather than a decrease in glutamate uptake, while biochemical studies4,17,18 have suggested that the increase in release persists for several hours. Morphological studies have described early but persistent increases in the spine number5,14 and area.28 Increases in the number of segmented/perforated synapses persisting for at least 1 h after induction of Long-Term Potentiation, have also been reported.9,24 These morphological changes suggest both presynaptic and postsynaptic modifications.15 Increases in synaptic vesicle number20 and distribution1 lasting for at least 1 h specifically indicate presynaptic changes. To explore further the role of the presynaptic Terminal in Long-Term Potentiation, we have investigated changes in three synaptic vesicle proteins, synapsin, synaptotagmin and synaptophysin, in control tissue and in tissue prepared from potentiated dentate gyrus 45 min and 3 h after induction of Long-Term Potentiation. We found that there was an increase in the concentration of the three proteins 3 h after induction of Long-Term Potentiation. No such increase was observed 45 min after induction or in tissue prepared from animals in which an intraventricular injection of the N-methyl-d-aspartate receptor antagonist, D(−)-2-amino-5-phosphonopentanoic acid, blocked induction of Long-Term Potentiation. This finding demonstrates an increased expression of synaptic vesicle proteins in Long-Term Potentiation and implies the existence of distinct temporal phases of Long-Term Potentiation during which different synaptic mechanisms for increased transmitter release are engaged.
Roger A. Nicoll - One of the best experts on this subject based on the ideXlab platform.
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a brief history of Long Term Potentiation
Neuron, 2017Co-Authors: Roger A. NicollAbstract:Since the discovery of Long-Term Potentiation (LTP) in 1973, thousands of papers have been published on this intriguing phenomenon, which provides a compelling cellular model for learning and memory. Although LTP has suffered considerable growing pains over the years, LTP has finally come of age. Here the rich history of LTP is reviewed. These are exciting times and the pace of discovery is remarkable.
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Long Term Potentiation a decade of progress
Science, 1999Co-Authors: Robert C Malenka, Roger A. NicollAbstract:Long-Term Potentiation of synaptic transmission in the hippocampus is the leading experimental model for the synaptic changes that may underlie learning and memory. This review presents a current understanding of the molecular mechanisms of this Long-lasting increase in synaptic strength and describes a simple model that unifies much of the data that previously were viewed as contradictory.
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Postsynaptic Membrane Fusion and Long-Term Potentiation
Science, 1998Co-Authors: Pierre-marie Lledo, Xiangyang Zhang, Robert C Malenka, Thomas C Sudhof, Roger A. NicollAbstract:The possibility that membrane fusion events in the postsynaptic cell may be required for the change in synaptic strength resulting from Long-Term Potentiation (LTP) was examined. Introducing substances into the postsynaptic cell that block membrane fusion at a number of different steps reduced LTP. Introducing SNAP, a protein that promotes membrane fusion, into cells enhanced synaptic transmission, and this enhancement was significantly less when generated in synapses that expressed LTP. Thus, postsynaptic fusion events, which could be involved either in retrograde signaling or in regulating postsynaptic receptor function or both, contribute to LTP.
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postsynaptic contribution to Long Term Potentiation revealed by the analysis of miniature synaptic currents
Nature, 1992Co-Authors: Toshiya Manabe, Pius Renner, Roger A. NicollAbstract:Miniature excitatory synaptic currents were recorded from CA1 pyramidal cells in hippocampal slices to study the site of the persistent change in synaptic efficacy during Long-Term Potentiation. Induction of Long-Term Potentiation produced a large increase in the amplitude of these currents. Such a change in amplitude suggests an increase in postsynaptic transmitter sensitivity.
Graham L Collingridge - One of the best experts on this subject based on the ideXlab platform.
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transient incorporation of native glur2 lacking ampa receptors during hippocampal Long Term Potentiation
Nature Neuroscience, 2006Co-Authors: Karen Plant, Graham L Collingridge, Kenneth A Pelkey, Zuner A Bortolotto, Daiju Morita, Akira Terashima, Chris J Mcbain, John T R IsaacAbstract:Transient incorporation of native GluR2-lacking AMPA receptors during hippocampal Long-Term Potentiation
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A synaptic model of memory: Long-Term Potentiation in the hippocampus.
Nature, 1993Co-Authors: Timothy V P Bliss, Graham L CollingridgeAbstract:Long-Term Potentiation of synaptic transmission in the hippocampus is the primary experimental model for investigating the synaptic basis of learning and memory in vertebrates. The best understood form of Long-Term Potentiation is induced by the activation of the N-methyl-D-aspartate receptor complex. This subtype of glutamate receptor endows Long-Term Potentiation with Hebbian characteristics, and allows electrical events at the postsynaptic membrane to be transduced into chemical signals which, in turn, are thought to activate both pre- and postsynaptic mechanisms to generate a persistent increase in synaptic strength.
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Synaptic plasticity: Long-Term Potentiation in the hippocampus
Current Opinion in Neurobiology, 1992Co-Authors: Zafar I. Bashir, Graham L CollingridgeAbstract:Abstract Advances in the past year have provided new information concerning the involvement of the metabotropic glutamate receptor in Long-Term Potentiation and the possible role of nitric oxide as a retrograde messenger.
Charles F. Zorumski - One of the best experts on this subject based on the ideXlab platform.
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Effects of insulin on Long-Term Potentiation in hippocampal slices from diabetic rats.
Diabetologia, 2003Co-Authors: Yukitoshi Izumi, Kelvin A. Yamada, Mio Matsukawa, Charles F. ZorumskiAbstract:Aims/Hypothesis Cognitive deficits occur commonly in diabetic patients. It is unclear whether these impairments result from hypoglycaemia during intensive insulin therapy, or from the diabetes itself. The aim of this study was to examine if impaired energy utilization resulting from insulin deficiency contributes to impaired Long-Term Potentiation (reflecting impaired synaptic plasticity). As Long-Term Potentiation is considered a candidate cellular mechanism underlying learning and memory, understanding how diabetes alters Long-Term Potentiation may provide insight into mechanisms producing cognitive deficits in diabetes.
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Arachidonic acid rescues hippocampal Long-Term Potentiation blocked by group I metabotropic glutamate receptor antagonists
Neuroscience, 2000Co-Authors: Yukitoshi Izumi, A.r Zarrin, Charles F. ZorumskiAbstract:Abstract Although there is evidence that group I metabotropic glutamate receptors participate in Long-Term Potentiation, the role of these receptors remains unclear. Among antagonists of group I metabotropic glutamate receptors, the mGluR5-selective 6-methyl-2-(phenylethynyl)-pyridine inhibited Long-Term Potentiation in the CA1 region of hippocampal slices from 30-day-old rats, whereas (RS)-1-aminoindan-1,5-dicarboxylic acid and cyclopropan[b]chromen-1a-carboxylic acid ethylester, which are more selective for mGluR1, failed to inhibit Long-Term Potentiation. Evidence also indicates that arachidonic acid is required for Long-Term Potentiation, as inhibition of phospholipase A 2 blocks Long-Term Potentiation. Administration of arachidonic acid immediately after tetanic stimulation restored Long-Term Potentiation that had been inhibited by group I antagonists. Furthermore, arachidonic acid overcame inhibition of Long-Term Potentiation by xestospongin C, an inositol triphosphate receptor channel blocker, or by thapsigargin, an agent that depletes intracellular calcium stores. However, arachidonic acid did not restore Long-Term Potentiation blocked by N -methyl- d -aspartate receptor antagonists. Although it has been assumed that the source of the arachidonic acid necessary for Long-Term Potentiation is N -methyl- d -aspartate receptor activation, our results suggest that during Long-Term Potentiation group I metabotropic glutamate receptors cause arachidonic acid release by mobilization of intracellular calcium.
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Long-Term Potentiation during whole-cell recording in rat hippocampal slices.
Neuroscience, 1993Co-Authors: K. Kato, David B. Clifford, Charles F. ZorumskiAbstract:Abstract Factors involved in the production of Long-Term Potentiation in the CA1 region of rat hippocampal slices were examined using whole-cell voltage clamp recordings. The pairing of postsynaptic membrane depolarization with tetanic stimulation produced a reliable Long-lasting enhancement of synaptic currents provided that the pairing was performed within 15 min after establishing intracellular contact. This time could be extended to 30 min by including adenosine triphosphate and guanosine triphosphate in the recording pipette. Once established, the Potentiation persisted for 3 h or more. The washout of Long-Term Potentiation generating ability was not correlated with a rundown in baseline synaptic currents or in the N -methyl- d -aspartate receptor-mediated component of synaptic responses, but followed a time course similar to the loss of calcium spikes. Long-Term Potentiation could be reliably produced by depolarizing the postsynaptic membrane to −40 or − 20 mV during the tetanus, but decreased when the membrane was held at membrane potentials greater than 0mV. At − 20 mV, 50 μM 2-amino-5-phosphonovalerate blocked the Potentiation but this agent was ineffective at +40 mV. In contrast, 50 μM verapamil, a calcium channel blocker, failed to alter Long-Term Potentiation at −20 mV but blocked the enhancement at +40mV. These results suggest that whole-cell recording causes a washout of postsynaptic factors important in the initiation of Long-Term Potentiation. However, these factors are less important in maintaining the Potentiation. Furthermore, depending on the postsynaptic membrane potential during tetanic stimulation, voltage-gated calcium channels contribute to CA1 Long-Term Potentiation.
Tim V. P. Bliss - One of the best experts on this subject based on the ideXlab platform.
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Long-Term Potentiation in the dentate gyrus: induction and increased glutamate release are blocked by D(-)aminophosphonovalerate.
Neuroscience, 2003Co-Authors: M.l. Errington, Marina A Lynch, Tim V. P. BlissAbstract:Abstract d (−)Aminophosphonovalerate, a specific antagonist of the N-methyl- d -aspartate subtype of glutamate receptor, was perfused through a push-pull cannula into the dentate gyrus of rats anaesthetized with urethan in order to observe its effect on the induction and maintenance of Long-Term Potentiation and on the increase in release of endogenous glutamate associated with Long-Term Potentiation. The amplitude of the population spike evoked by single test shocks to the perforant path was significantly depressed by 100 μM d (−)aminophosphonovalerate, but there was a minimal effect on the slope of the population excitatory postsynaptic potential, or on the concentration of glutamate released into the perfusate. A brief high-intensity tetanus given to the perforant path while d (−)aminophosphonovalerate was being perfused failed to induce Long-Term Potentiation or the sustained increase in glutamate release associated with Long-Term Potentiation. Short-Term post-tetanic Potentiation was not affected. After wash-out of d (−)aminophosphonovalerate, a second high-frequency train produced both Long-Term Potentiation and an increase in glutamate release which was sustained for the subsequent l h period of observation. d (−)Aminophosphonovalerate did not suppress Long-Term Potentiation once it had been induced. d (−)Aminophosphonovalerate (100 μM) did not itself affect in vivo release of glutamate. However, in a separate series of in vitro experiments, d (−)aminophosphonovalerate at concentrations of 50 μ M and above was found to depress the Ca 2+ -dependent, K + -stimulated release of preloaded [ 14 C]-glutamate from dentate slices. These results suggest that in the dentate gyrus activation of the N-methyl- d -aspartate receptor is required for the induction though not the maintenance of Long-Term Potentiation. The possibility that presynaptic mechanisms contribute to the suppression of Long-Term Potentiation should not be overlooked in view of our in vitro data. The further demonstration in these experiments that a high-frequency train produces a sustained increase in glutamate release only when it also produces Long-Term Potentiation provides additional evidence for the view that the maintenance of Long-Term Potentiation is due, at least in part, to a presynaptic mechanism.
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Long-Term Potentiation in awake mutant mice.
Nature, 1997Co-Authors: M.l. Errington, Tim V. P. Bliss, Richard W Morris, Serge Laroche, Sabrina DavisAbstract:The relationship between Long-Term Potentiation (LTP) and spatial learning has been explored in a variety of genetically engineered mice with deletions of specific genes1. With few exceptions, LTP in these animals has been studied in the hippocampal slice preparation. The conditions required to elicit LTP in vitro, however, may not be comparable to those in the intact animal.
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Increase in synaptic vesicle proteins accompanies Long-Term Potentiation in the dentate gyrus
Neuroscience, 1994Co-Authors: Marina A Lynch, K. L. Voss, J. Rodriguez, Tim V. P. BlissAbstract:Maintenance of Long-Term Potentiation in synapses formed by the perforant path on to granule cells of the dentate gyrus is accompanied by a sustained increase in the extracellular concentration of glutamate,3,4 the presumed transmitter at this excitatory hippocampal pathway. Quantal analysis2,12,13,19,27 indicates that, at least in the first hour of induction, this reflects an increase in transmitter release rather than a decrease in glutamate uptake, while biochemical studies4,17,18 have suggested that the increase in release persists for several hours. Morphological studies have described early but persistent increases in the spine number5,14 and area.28 Increases in the number of segmented/perforated synapses persisting for at least 1 h after induction of Long-Term Potentiation, have also been reported.9,24 These morphological changes suggest both presynaptic and postsynaptic modifications.15 Increases in synaptic vesicle number20 and distribution1 lasting for at least 1 h specifically indicate presynaptic changes. To explore further the role of the presynaptic Terminal in Long-Term Potentiation, we have investigated changes in three synaptic vesicle proteins, synapsin, synaptotagmin and synaptophysin, in control tissue and in tissue prepared from potentiated dentate gyrus 45 min and 3 h after induction of Long-Term Potentiation. We found that there was an increase in the concentration of the three proteins 3 h after induction of Long-Term Potentiation. No such increase was observed 45 min after induction or in tissue prepared from animals in which an intraventricular injection of the N-methyl-d-aspartate receptor antagonist, D(−)-2-amino-5-phosphonopentanoic acid, blocked induction of Long-Term Potentiation. This finding demonstrates an increased expression of synaptic vesicle proteins in Long-Term Potentiation and implies the existence of distinct temporal phases of Long-Term Potentiation during which different synaptic mechanisms for increased transmitter release are engaged.
