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Mark F. Bear - One of the best experts on this subject based on the ideXlab platform.
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Chemical Induction of mGluR5- and Protein Synthesis–Dependent Long-Term Depression in Hippocampal Area CA1
Journal of neurophysiology, 2001Co-Authors: Kimberly M Huber, John C Roder, Mark F. BearAbstract:Recent work has demonstrated that specific patterns of synaptic stimulation can induce Long-Term Depression (LTD) in area CA1 that depends on activation of metabotropic glutamate receptors (mGluRs)...
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chemical induction of mglur5 and protein synthesis dependent Long Term Depression in hippocampal area ca1
Journal of Neurophysiology, 2001Co-Authors: Kimberly M Huber, John C Roder, Mark F. BearAbstract:Recent work has demonstrated that specific patterns of synaptic stimulation can induce Long-Term Depression (LTD) in area CA1 that depends on activation of metabotropic glutamate receptors (mGluRs)...
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Long-Term Depression in Hippocampus
Annual review of neuroscience, 1996Co-Authors: Mark F. Bear, Wickliffe C. AbrahamAbstract:Long-Term Depression (LTD) is a lasting decrease in synaptic effectiveness that follows some types of electrical stimulation in the hippocampus. Two broad types of LTD may be distinguished. Heterosynaptic LTD can occur at synapses that are inactive, normally during high-frequency stimulation of a converging synaptic input. Homosynaptic LTD can occur at synapses that are activated, normally at low frequencies. Here we discuss the mechanisms of LTD and their possible relevance to hippocampal function.
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Homosynaptic Long-Term Depression in the visual cortex.
The Journal of Neuroscience, 1994Co-Authors: Alfredo Kirkwood, Mark F. BearAbstract:We have investigated the characteristics and mechanism of activity- dependent decreases in synaptic effectiveness in visual cortex. Repetitive, low-frequency stimulation (LFS) of either layer IV or the white matter of visual cortical slices was shown to result in a Long- Term Depression (LTD) of intra- and extracellularly recorded synaptic responses in layer III. In preparations in which responses to stimulation of two independent pathways could be monitored, LFS of one pathway produced LTD of responses to test stimulation of that input only, showing that this form of LTD is homosynaptic. This form of LTD was dependent on the frequency and/or pattern of conditioning stimulation and on activation of NMDA receptors. Okadaic acid, an inhibitor of protein phosphatases 1 and 2a, inhibited LTD, but had no effect on induction of Long-Term potentiation. In all of these respects, LFS-induced LTD in visual cortex closely resembles what has been recently documented in hippocampus. The combined data support a model in which LTD is triggered by a modest elevation in postsynaptic Ca2+ and activation of protein-serine, threonine phosphatases.
Stephanie L Borgland - One of the best experts on this subject based on the ideXlab platform.
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insulin induces Long Term Depression of ventral tegmental area dopamine neurons via endocannabinoids
Nature Neuroscience, 2013Co-Authors: Gwenael Labouebe, Carine Dias, Jovi C Y Wong, Subashini Karunakaran, Susanne M Clee, Anthony G Phillips, Benjamin Boutrel, Stephanie L BorglandAbstract:The authors show that insulin induces Long-Term Depression of excitatory synapses onto ventral tegmental area (VTA) neurons in rodents, which requires endocannabinoid-mediated presynaptic inhibition of glutamate release. Insulin infusion into the VTA reduces food anticipatory behavior and conditioned place preference for food, suggesting a role for this plasticity in behavior.
Zafar I. Bashir - One of the best experts on this subject based on the ideXlab platform.
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BRAGging about mechanisms of Long-Term Depression.
Neuron, 2010Co-Authors: Stephen M. Fitzjohn, Zafar I. BashirAbstract:The mechanisms of Long-Term Depression (LTD) underlie various aspects of normal brain function. Therefore, it is important to understand the signaling that underpins LTD. The study by Scholz et al. in this issue of Neuron describes how BRAG2, mGluRs, and AMPARs come together to produce LTD through AMPAR internalization.
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Expression of Long-Term Depression Underlies Visual Recognition Memory
Neuron, 2008Co-Authors: Sarah Griffiths, Helen L. Scott, Alison S. Bienemann, Colin P J Glover, Malcolm W. Brown, Mohamed T Ghorbel, E. Clea Warburton, James B Uney, Zafar I. BashirAbstract:Summary The modifications occurring in the brain during learning and memory are still poorly understood but may involve Long-lasting changes in synaptic transmission (synaptic plasticity). In perirhinal cortex, a lasting decrement in neuronal responsiveness is associated with visual familiarity discrimination, leading to the hypothesis that Long-Term Depression (LTD)-like synaptic plasticity may underlie recognition memory. LTD relies on internalization of AMPA receptors (AMPARs) through interaction between their GluR2 subunits and AP2, the clathrin adaptor protein required for endocytosis. We demonstrate that a peptide that blocks interactions between GluR2 and AP2 blocks LTD in perirhinal cortex in vitro. Viral transduction of this peptide in perirhinal cortex produced striking deficits in visual recognition memory. Furthermore, there was a deficit of LTD in perirhinal cortex slices from virally transduced, recognition memory-deficient animals. These results suggest that internalization of AMPA receptors, a process critical for the expression of LTD in perirhinal cortex, underlies visual recognition memory.
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Long-Term Depression: multiple forms and implications for brain function
Trends in neurosciences, 2007Co-Authors: Peter V. Massey, Zafar I. BashirAbstract:Long-Term potentiation (LTP) and Long-Term Depression (LTD) remain widely accepted vertebrate models for the cellular and molecular mechanisms that underlie synaptic changes during learning and memory. Although LTD is a phenomenon that occurs in many regions of the CNS, it is clear that the mechanisms recruited in its induction and expression can vary, depending on many factors, including brain region and developmental time point. LTD in the hippocampus and cerebellum is probably the best characterized, although there are also other brain areas where mechanisms of LTD are well understood, and where it is thought to have a functional role.
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On Long-Term Depression induced by activation of G-protein coupled receptors.
Neuroscience research, 2003Co-Authors: Zafar I. BashirAbstract:In this mini-review I consider the mechanisms by which activation of glutamate and acetylcholine metabotropic receptors can result in the induction of Long-Term Depression. Two regions of the CNS will receive particular attention; the CA1 region of hippocampus and the perirhinal cortex.
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Long-Term Depression: a cascade of induction and expression mechanisms.
Progress in neurobiology, 2001Co-Authors: Nicola Kemp, Zafar I. BashirAbstract:The aims of this paper are to provide a comprehensive and up to date review of the mechanisms of induction and expression of Long-Term Depression (LTD) of synaptic transmission. The review will focus largely on homosynaptic LTD and other forms of LTD will be considered only where appropriate for a fuller understanding of LTD mechanisms. We shall concentrate on what are felt to be some of the most interesting recent findings concerning LTD in the central nervous system. Wherever possible we shall try to consider some of the disparities in results and possible reasons for these. Finally, we shall briefly consider some of the possible functional consequences of LTD for normal physiological function.
Tomoo Hirano - One of the best experts on this subject based on the ideXlab platform.
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Intracellular Ca2+ thresholds for induction of excitatory Long-Term Depression and inhibitory Long-Term potentiation in a cerebellar Purkinje neuron
Biochemical and biophysical research communications, 2015Co-Authors: Yoji Nakamura, Tomoo HiranoAbstract:Synaptic plasticity in the cerebellar cortex contributes to motor learning. In particular, Long-Term Depression at excitatory parallel fiber - Purkinje neuron synapses has been intensively studied as a primary cellular mechanism for motor learning. Recent studies showed that synaptic plasticity other than Long-Term Depression such as Long-Term potentiation at inhibitory interneuron - Purkinje neuron synapses called rebound potentiation is also involved in motor learning. It was suggested that Long-Term Depression and rebound potentiation might synergistically support motor learning. Here, we have examined induction conditions of Long-Term Depression and rebound potentiation in cultured rat Purkinje neurons, and found that both of them were induced simultaneously by certain patterns of depolarization of a Purkinje neuron. Further, we found that Long-Term Depression was induced by shorter depolarizing pulses causing a smaller intracellular Ca(2+) increase than rebound potentiation. These results support an idea that Long-Term Depression and rebound potentiation synergistically contribute to motor learning, and suggest that Long-Term Depression may play a primary role in wider variety of motor learning paradigms than rebound potentiation.
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Involvement of inositol trisphosphate in cerebellar Long-Term Depression.
Neuroreport, 1995Co-Authors: Keizo Kasono, Tomoo HiranoAbstract:We examined the role of increases in Ca 2+ from different sources in the induction of Long-Term Depression (LTD) of glutamate or AMPA responsiveness in cultured Purkinje neurones. Photolysis of caged Ca 2+ or caged inositol 1,4,5-trisphosphate (InsP 3 ) as well as depolarisation was used to increase Ca 2+ concentration. Heparin, contained in a patch pipette to block InsP 3 binding to its receptor, prevented LTD induction by coupling of glutamate application and depolarisation. Although pairing of depolarisation and AMPA application did not induce LTD, photolysis of caged InsP 3 in conjunction with depolarisation and AMPA application induced LTD. The results suggest that not only Ca 2+ influx through voltage-gated Ca channels but also InsP 3 -induced Ca 2+ mobilisation are involved in LTD induction
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Antibodies inactivating mGluR1 metabotropic glutamate receptor block Long-Term Depression in cultured Purkinje cells
Neuron, 1994Co-Authors: Ryuichi Shigemoto, Takaaki Abe, Sakashi Nomura, Shigetada Nakanishi, Tomoo HiranoAbstract:Abstract Antibodies were raised against two distinct extracellular sequences of the rat mGIuR1 metabotropic glutamate receptor expressed as bacterial fusion proteins. Both antibodies specifically reacted with mGIuR1 in the rat cerebellum and inhibited the mGIuR1 activity as assessed by the analysis of glutamate-stimulated inositol phosphate formation in CHO cells expressing mGIuR1. Using these antibodies, we examined the role of mGIuR1 in the induction of Long-Term Depression in cultured Purkinje cells. In voltage-clamped Purkinje cells, current induced by iontophoretically applied glutamate was persistently depressed by depolarization of the Purkinje cells in conjunction with the glutamate application. The mGIuR1 antibodies completely blocked the Depression of glutamate-induced current. The results indicate that activation of mGIuR1 is necessary for the induction of cerebellar Long-Term Depression and that these mGIuR1 antibodies can be used as selective antagonists.
Masao Ito - One of the best experts on this subject based on the ideXlab platform.
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Long-Term Depression: Cerebellum
Encyclopedia of Neuroscience, 2009Co-Authors: Masao ItoAbstract:Long-Term Depression (LTD) is a persistent decrease in synaptic efficacy that occurs in an activity-dependent manner. LTD synergistically functions with Long-Term potentiation (LTP) to generate a balanced, stable memory mechanism. Although LTP plays a major role in the associative type of learning that occurs in the hippocampus and neocortex, LTD is a major player in the error-driven learning that occurs in the cerebellar cortex. Recent studies have revealed complex signal transduction processes underlying LTD. In the Long run, LTD may lead to a loss of synapses, or to preservation as silent synapses that have recently been found to prevail in the cerebellar cortex.
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The molecular organization of cerebellar Long-Term Depression
Nature reviews. Neuroscience, 2002Co-Authors: Masao ItoAbstract:Synaptic plasticity is an important cellular mechanism for the formation of memory in neuronal circuits of the brain. Research during the past two decades has revealed surprisingly complex signal-transduction processes that underlie various forms of synaptic plasticity. More than 30 molecules are involved in the induction of Long-Term Depression (LTD) — a unique form of synaptic plasticity in the cerebellum. Here, I review recent data on these molecules, defining their roles as mediators or modulators, coincidence detectors or components of a self-regenerating circuit, and show how they are organized to form an efficient molecular machinery for LTD induction.
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Cerebellar Long-Term Depression: Characterization, Signal Transduction, and Functional Roles
Physiological reviews, 2001Co-Authors: Masao ItoAbstract:Cerebellar Purkinje cells exhibit a unique type of synaptic plasticity, namely, Long-Term Depression (LTD). When two inputs to a Purkinje cell, one from a climbing fiber and the other from a set of...
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Long-Term Depression (Cerebellum)
International Encyclopedia of the Social & Behavioral Sciences, 2001Co-Authors: Masao ItoAbstract:Long-Term Depression (LTD) displayed in the cerebellar cortex is a persistent decrease of the transmission efficacy from granule cell to Purkinje cells. LTD is induced when two inputs to a Purkinje cell, one from a climbing fiber and the other from a set of granule cell axons, are repeatedly associated. This article defines the physiological characteristics of LTD and reviews recent findings of complex signal transduction processes, which underlie LTD, involving a variety of substances that eventually lead to the inactivation of ionotropic glutamate receptors. Evidence also indicates that climbing fibers convey error signals, not only for an error consequent to a movement but also for errors arising from control mechanisms in the central nervous system. LTD is thus thought to play a key role in reorganization of the neuronal network of the cerebellum by depressing those granule cell–Purkinje cell synapses that are activated in association with errors. This view has been supported by showing that pharmacological or genetic inhibition of LTD impairs various forms of motor learning.
