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Roger A. Nicoll - One of the best experts on this subject based on the ideXlab platform.

  • adenosine gates synaptic plasticity at Hippocampal Mossy Fiber synapses
    Proceedings of the National Academy of Sciences of the United States of America, 2003
    Co-Authors: Kimberly A Moore, Roger A. Nicoll, Dietmar Schmitz
    Abstract:

    The release properties of synapses in the central nervous system vary greatly, not only across anatomically distinct types of synapses but also among the same class of synapse. This variation manifests itself in large part by differences in the probability of transmitter release, which affects such activity-dependent presynaptic forms of plasticity as paired-pulse facilitation and frequency facilitation. This heterogeneity in presynaptic function reflects differences in the intrinsic properties of the synaptic terminal and the activation of presynaptic neurotransmitter receptors. Here we show that the unique presynaptic properties of the Hippocampal Mossy Fiber synapse are largely imparted onto the synapse by the continuous local action of extracellular adenosine at presynaptic A1 adenosine receptors, which maintains a low basal probability of transmitter release.

  • presynaptic kainate receptors impart an associative property to Hippocampal Mossy Fiber long term potentiation
    Nature Neuroscience, 2003
    Co-Authors: Dietmar Schmitz, Joerg Breustedt, Jack R Mellor, Roger A. Nicoll
    Abstract:

    Hippocampal Mossy Fiber synapses show an unusual form of long-term potentiation (LTP) that is independent of NMDA receptor activation and is expressed presynaptically. Using receptor antagonists, as well as receptor knockout mice, we found that presynaptic kainate receptors facilitate the induction of Mossy Fiber long-term potentiation (LTP), although they are not required for this form of LTP. Most importantly, these receptors impart an associativity to Mossy Fiber LTP such that activity in neighboring Mossy Fiber synapses, or even associational/commissural synapses, influences the threshold for inducing Mossy Fiber LTP. Such a mechanism greatly increases the computational power of this form of plasticity.

  • mediation of Hippocampal Mossy Fiber long term potentiation by presynaptic ih channels
    Science, 2002
    Co-Authors: Jack R Mellor, Roger A. Nicoll, Dietmar Schmitz
    Abstract:

    Hippocampal Mossy Fiber long-term potentiation (LTP) is expressed presynaptically, but the exact mechanisms remain unknown. Here, we demonstrate the involvement of the hyperpolarization-activated cation channel (Ih) in the expression of Mossy Fiber LTP. Established LTP was blocked and reversed by Ih channel antagonists. Whole-cell recording from granule cells revealed that repetitive stimulation causes a calcium- and Ih-dependent long-lasting depolarization mediated by protein kinase A. Depolarization at the terminals would be expected to enhance transmitter release, whereas somatic depolarization would enhance the responsiveness of granule cells to afferent input. Thus, Ih channels play an important role in the long-lasting control of transmitter release and neuronal excitability.

  • presynaptic kainate receptors at Hippocampal Mossy Fiber synapses
    Proceedings of the National Academy of Sciences of the United States of America, 2001
    Co-Authors: Dietmar Schmitz, Jack R Mellor, Matthew Frerking, Roger A. Nicoll
    Abstract:

    Hippocampal Mossy Fibers, which are the axons of dentate granule cells, form powerful excitatory synapses onto the proximal dendrites of CA3 pyramidal cells. It has long been known that high-affinity binding sites for kainate, a glutamate receptor agonist, are present on Mossy Fibers. Here we summarize recent experiments on the role of these presynaptic kainate receptors (KARs). Application of kainate has a direct effect on the amplitude of the extracellularly recorded Fiber volley, with an enhancement by low concentrations and a depression by high concentrations. These effects are mediated by KARs, because they persist in the presence of the alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor-selective antagonist GYKI 53655, but are blocked by the alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid/KAR antagonist 6-cyano-7-nitroquinoxaline-2,3-dione and the KAR antagonist SYM2081. The effects on the Fiber volley are most likely caused by a depolarization of the Fibers via the known ionotropic actions of KARs, because application of potassium mimics the effects. In addition to these effects on Fiber excitability, low concentrations of kainate enhance transmitter release, whereas high concentrations depress transmitter release. Importantly, the synaptic release of glutamate from Mossy Fibers also activates these presynaptic KARs, causing an enhancement of the Fiber volley and a facilitation of release that lasts for many seconds. This positive feedback contributes to the dramatic frequency facilitation that is characteristic of Mossy Fiber synapses. It will be interesting to determine how widespread facilitatory presynaptic KARs are at other synapses in the central nervous system.

  • presynaptic kainate receptor mediation of frequency facilitation at Hippocampal Mossy Fiber synapses
    Science, 2001
    Co-Authors: Dietmar Schmitz, Jack R Mellor, Roger A. Nicoll
    Abstract:

    Inhibition of transmitter release by presynaptic receptors is widespread in the central nervous system and is typically mediated via metabotropic receptors. In contrast, very little is known about facilitatory receptors, and synaptic activation of a facilitatory autoreceptor has not been established. Here we show that activation of presynaptic kainate receptors can facilitate transmitter release from Hippocampal Mossy Fiber synapses. Synaptic activation of these presumed ionotropic kainate receptors is very fast (<10 ms) and lasts for seconds. Thus, these presynaptic kainate receptors contribute to the short-term plasticity characteristics of Mossy Fiber synapses, which were previously thought to be an intrinsic property of the synapse.

Dietmar Schmitz - One of the best experts on this subject based on the ideXlab platform.

  • Recruitment of release sites underlies chemical presynaptic potentiation at Hippocampal Mossy Fiber boutons.
    'Public Library of Science (PLoS)', 2021
    Co-Authors: Marta Orlando, Marta Maglione, Stephan J Sigrist, Anton Dvorzhak, Felicitas Bruentgens, Benjamin R Rost, Jörg Breustedt, Dietmar Schmitz
    Abstract:

    Synaptic plasticity is a cellular model for learning and memory. However, the expression mechanisms underlying presynaptic forms of plasticity are not well understood. Here, we investigate functional and structural correlates of presynaptic potentiation at large Hippocampal Mossy Fiber boutons induced by the adenylyl cyclase activator forskolin. We performed 2-photon imaging of the genetically encoded glutamate sensor iGluu that revealed an increase in the surface area used for glutamate release at potentiated terminals. Time-gated stimulated emission depletion microscopy revealed no change in the coupling distance between P/Q-type calcium channels and release sites mapped by Munc13-1 cluster position. Finally, by high-pressure freezing and transmission electron microscopy analysis, we found a fast remodeling of synaptic ultrastructure at potentiated boutons: Synaptic vesicles dispersed in the terminal and accumulated at the active zones, while active zone density and synaptic complexity increased. We suggest that these rapid and early structural rearrangements might enable long-term increase in synaptic strength

  • adenosine gates synaptic plasticity at Hippocampal Mossy Fiber synapses
    Proceedings of the National Academy of Sciences of the United States of America, 2003
    Co-Authors: Kimberly A Moore, Roger A. Nicoll, Dietmar Schmitz
    Abstract:

    The release properties of synapses in the central nervous system vary greatly, not only across anatomically distinct types of synapses but also among the same class of synapse. This variation manifests itself in large part by differences in the probability of transmitter release, which affects such activity-dependent presynaptic forms of plasticity as paired-pulse facilitation and frequency facilitation. This heterogeneity in presynaptic function reflects differences in the intrinsic properties of the synaptic terminal and the activation of presynaptic neurotransmitter receptors. Here we show that the unique presynaptic properties of the Hippocampal Mossy Fiber synapse are largely imparted onto the synapse by the continuous local action of extracellular adenosine at presynaptic A1 adenosine receptors, which maintains a low basal probability of transmitter release.

  • presynaptic kainate receptors impart an associative property to Hippocampal Mossy Fiber long term potentiation
    Nature Neuroscience, 2003
    Co-Authors: Dietmar Schmitz, Joerg Breustedt, Jack R Mellor, Roger A. Nicoll
    Abstract:

    Hippocampal Mossy Fiber synapses show an unusual form of long-term potentiation (LTP) that is independent of NMDA receptor activation and is expressed presynaptically. Using receptor antagonists, as well as receptor knockout mice, we found that presynaptic kainate receptors facilitate the induction of Mossy Fiber long-term potentiation (LTP), although they are not required for this form of LTP. Most importantly, these receptors impart an associativity to Mossy Fiber LTP such that activity in neighboring Mossy Fiber synapses, or even associational/commissural synapses, influences the threshold for inducing Mossy Fiber LTP. Such a mechanism greatly increases the computational power of this form of plasticity.

  • mediation of Hippocampal Mossy Fiber long term potentiation by presynaptic ih channels
    Science, 2002
    Co-Authors: Jack R Mellor, Roger A. Nicoll, Dietmar Schmitz
    Abstract:

    Hippocampal Mossy Fiber long-term potentiation (LTP) is expressed presynaptically, but the exact mechanisms remain unknown. Here, we demonstrate the involvement of the hyperpolarization-activated cation channel (Ih) in the expression of Mossy Fiber LTP. Established LTP was blocked and reversed by Ih channel antagonists. Whole-cell recording from granule cells revealed that repetitive stimulation causes a calcium- and Ih-dependent long-lasting depolarization mediated by protein kinase A. Depolarization at the terminals would be expected to enhance transmitter release, whereas somatic depolarization would enhance the responsiveness of granule cells to afferent input. Thus, Ih channels play an important role in the long-lasting control of transmitter release and neuronal excitability.

  • presynaptic kainate receptors at Hippocampal Mossy Fiber synapses
    Proceedings of the National Academy of Sciences of the United States of America, 2001
    Co-Authors: Dietmar Schmitz, Jack R Mellor, Matthew Frerking, Roger A. Nicoll
    Abstract:

    Hippocampal Mossy Fibers, which are the axons of dentate granule cells, form powerful excitatory synapses onto the proximal dendrites of CA3 pyramidal cells. It has long been known that high-affinity binding sites for kainate, a glutamate receptor agonist, are present on Mossy Fibers. Here we summarize recent experiments on the role of these presynaptic kainate receptors (KARs). Application of kainate has a direct effect on the amplitude of the extracellularly recorded Fiber volley, with an enhancement by low concentrations and a depression by high concentrations. These effects are mediated by KARs, because they persist in the presence of the alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor-selective antagonist GYKI 53655, but are blocked by the alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid/KAR antagonist 6-cyano-7-nitroquinoxaline-2,3-dione and the KAR antagonist SYM2081. The effects on the Fiber volley are most likely caused by a depolarization of the Fibers via the known ionotropic actions of KARs, because application of potassium mimics the effects. In addition to these effects on Fiber excitability, low concentrations of kainate enhance transmitter release, whereas high concentrations depress transmitter release. Importantly, the synaptic release of glutamate from Mossy Fibers also activates these presynaptic KARs, causing an enhancement of the Fiber volley and a facilitation of release that lasts for many seconds. This positive feedback contributes to the dramatic frequency facilitation that is characteristic of Mossy Fiber synapses. It will be interesting to determine how widespread facilitatory presynaptic KARs are at other synapses in the central nervous system.

Katalin Toth - One of the best experts on this subject based on the ideXlab platform.

  • slow decaying presynaptic calcium dynamics gate long lasting asynchronous release at the Hippocampal Mossy Fiber to ca3 pyramidal cell synapse
    Synapse, 2020
    Co-Authors: Simon Chamberland, Yulia Timofeeva, Alesya Evstratova, Christopher A Norman, Kirill E Volynski, Katalin Toth
    Abstract:

    Action potentials trigger two modes of neurotransmitter release, with a fast synchronous component and a temporally delayed asynchronous release. Asynchronous release contributes to information transfer at synapses, including at the Hippocampal Mossy Fiber (MF) to CA3 pyramidal cell synapse where it controls the timing of postsynaptic CA3 pyramidal neuron firing. Here, we identified and characterized the main determinants of asynchronous release at the MF-CA3 synapse. We found that asynchronous release at MF-CA3 synapses can last on the order of seconds following repetitive MF stimulation. Elevating the stimulation frequency or the external Ca2+ concentration increased the rate of asynchronous release, thus, arguing that presynaptic Ca2+ dynamics is the major determinant of asynchronous release rate. Direct MF bouton Ca2+ imaging revealed slow Ca2+ decay kinetics of action potential (AP) burst-evoked Ca2+ transients. Finally, we observed that asynchronous release was preferentially mediated by Ca2+ influx through P/Q-type voltage-gated Ca2+ channels, while the contribution of N-type VGCCs was limited. Overall, our results uncover the determinants of long-lasting asynchronous release from MF terminals and suggest that asynchronous release could influence CA3 pyramidal cell firing up to seconds following termination of granule cell bursting.

  • action potential counting at giant Mossy Fiber terminals gates information transfer in the hippocampus
    bioRxiv, 2017
    Co-Authors: Simon Chamberland, Yulia Timofeeva, Alesya Evstratova, Kirill E Volynski, Katalin Toth
    Abstract:

    Hippocampal Mossy Fiber terminals have long been recognized as conditional detonators owing to prominent short-term facilitation, but the patterns of activity required to fire postsynaptic CA3 pyramidal neurons remain poorly understood. We show that Mossy Fibers count the number of spikes to transmit information to CA3 pyramidal cells through a distinctive interplay between presynaptic calcium dynamics and vesicle replenishment. This identifies a previously unexplored information coding mechanism in the brain.

  • information processing and synaptic plasticity at Hippocampal Mossy Fiber terminals
    Frontiers in Cellular Neuroscience, 2014
    Co-Authors: Alesya Evstratova, Katalin Toth
    Abstract:

    Granule cells of the dentate gyrus receive cortical information and they transform and transmit this code to the CA3 area via their axons, the Mossy Fibers. Structural and functional complexity of this network has been extensively studied at various organizational levels. This review is focused on the anatomical and physiological properties of the Mossy Fiber system. We will discuss the mechanism by which dentate granule cells process signals from single action potentials, short bursts and longer stimuli. Various parameters of synaptic interactions at different target cells such as quantal transmission, short- and long-term plasticity will be summarized. Different types of synaptic contacts formed by Mossy Fibers have unique sets of rules for information processing during different rates of granule cell activity. We will investigate the complex interactions between key determinants of information transfer between the dentate gyrus and the CA3 area of the hippocampus.

Jack R Mellor - One of the best experts on this subject based on the ideXlab platform.

  • presynaptic kainate receptors impart an associative property to Hippocampal Mossy Fiber long term potentiation
    Nature Neuroscience, 2003
    Co-Authors: Dietmar Schmitz, Joerg Breustedt, Jack R Mellor, Roger A. Nicoll
    Abstract:

    Hippocampal Mossy Fiber synapses show an unusual form of long-term potentiation (LTP) that is independent of NMDA receptor activation and is expressed presynaptically. Using receptor antagonists, as well as receptor knockout mice, we found that presynaptic kainate receptors facilitate the induction of Mossy Fiber long-term potentiation (LTP), although they are not required for this form of LTP. Most importantly, these receptors impart an associativity to Mossy Fiber LTP such that activity in neighboring Mossy Fiber synapses, or even associational/commissural synapses, influences the threshold for inducing Mossy Fiber LTP. Such a mechanism greatly increases the computational power of this form of plasticity.

  • mediation of Hippocampal Mossy Fiber long term potentiation by presynaptic ih channels
    Science, 2002
    Co-Authors: Jack R Mellor, Roger A. Nicoll, Dietmar Schmitz
    Abstract:

    Hippocampal Mossy Fiber long-term potentiation (LTP) is expressed presynaptically, but the exact mechanisms remain unknown. Here, we demonstrate the involvement of the hyperpolarization-activated cation channel (Ih) in the expression of Mossy Fiber LTP. Established LTP was blocked and reversed by Ih channel antagonists. Whole-cell recording from granule cells revealed that repetitive stimulation causes a calcium- and Ih-dependent long-lasting depolarization mediated by protein kinase A. Depolarization at the terminals would be expected to enhance transmitter release, whereas somatic depolarization would enhance the responsiveness of granule cells to afferent input. Thus, Ih channels play an important role in the long-lasting control of transmitter release and neuronal excitability.

  • presynaptic kainate receptors at Hippocampal Mossy Fiber synapses
    Proceedings of the National Academy of Sciences of the United States of America, 2001
    Co-Authors: Dietmar Schmitz, Jack R Mellor, Matthew Frerking, Roger A. Nicoll
    Abstract:

    Hippocampal Mossy Fibers, which are the axons of dentate granule cells, form powerful excitatory synapses onto the proximal dendrites of CA3 pyramidal cells. It has long been known that high-affinity binding sites for kainate, a glutamate receptor agonist, are present on Mossy Fibers. Here we summarize recent experiments on the role of these presynaptic kainate receptors (KARs). Application of kainate has a direct effect on the amplitude of the extracellularly recorded Fiber volley, with an enhancement by low concentrations and a depression by high concentrations. These effects are mediated by KARs, because they persist in the presence of the alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor-selective antagonist GYKI 53655, but are blocked by the alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid/KAR antagonist 6-cyano-7-nitroquinoxaline-2,3-dione and the KAR antagonist SYM2081. The effects on the Fiber volley are most likely caused by a depolarization of the Fibers via the known ionotropic actions of KARs, because application of potassium mimics the effects. In addition to these effects on Fiber excitability, low concentrations of kainate enhance transmitter release, whereas high concentrations depress transmitter release. Importantly, the synaptic release of glutamate from Mossy Fibers also activates these presynaptic KARs, causing an enhancement of the Fiber volley and a facilitation of release that lasts for many seconds. This positive feedback contributes to the dramatic frequency facilitation that is characteristic of Mossy Fiber synapses. It will be interesting to determine how widespread facilitatory presynaptic KARs are at other synapses in the central nervous system.

  • presynaptic kainate receptor mediation of frequency facilitation at Hippocampal Mossy Fiber synapses
    Science, 2001
    Co-Authors: Dietmar Schmitz, Jack R Mellor, Roger A. Nicoll
    Abstract:

    Inhibition of transmitter release by presynaptic receptors is widespread in the central nervous system and is typically mediated via metabotropic receptors. In contrast, very little is known about facilitatory receptors, and synaptic activation of a facilitatory autoreceptor has not been established. Here we show that activation of presynaptic kainate receptors can facilitate transmitter release from Hippocampal Mossy Fiber synapses. Synaptic activation of these presumed ionotropic kainate receptors is very fast (<10 ms) and lasts for seconds. Thus, these presynaptic kainate receptors contribute to the short-term plasticity characteristics of Mossy Fiber synapses, which were previously thought to be an intrinsic property of the synapse.

  • Hippocampal Mossy Fiber LTP is independent of postsynaptic calcium
    Nature Neuroscience, 2001
    Co-Authors: Jack R Mellor, Roger A. Nicoll
    Abstract:

    We tested a proposal that postsynaptic calcium and metabotropic glutamate receptors (mGluRs) are involved in the induction of Hippocampal Mossy Fiber long-term potentiation (LTP)1. We found that blockade of mGluRs with a range of antagonists, or dialysis of the postsynaptic cell with 50 mM BAPTA, had no effect on Mossy Fiber LTP. Therefore, we concluded that Mossy Fiber LTP is independent of postsynaptic calcium.

German Barrionuevo - One of the best experts on this subject based on the ideXlab platform.

  • multiple forms of long term synaptic plasticity at Hippocampal Mossy Fiber synapses on interneurons
    Neuropharmacology, 2011
    Co-Authors: Emilio J Galvan, Kathleen E Cosgrove, German Barrionuevo
    Abstract:

    The Hippocampal Mossy Fiber (MF) pathway originates from the dentate gyrus granule cells and provides a powerful excitatory synaptic drive to neurons in the dentate gyrus hilus and area CA3. Much of the early work on the MF pathway focused on its electrophysiological properties, and ability to drive CA3 pyramidal cell activity. Over the last ten years, however, a new focus on the synaptic interaction between granule cells and inhibitory interneurons has emerged. These data have revealed an immense heterogeneity of long-term plasticity at MF synapses on various interneuron targets. Interestingly, these studies also indicate that the mechanisms of MF long-term plasticity in some interneuron subtypes may be more similar to pyramidal cells than previously appreciated. In this review, we first define the synapse types at each of the interneuron targets based on the receptors present. We then describe the different forms of long-term plasticity observed, and the mechanisms underlying each form as they are currently understood. Finally we highlight various open questions surrounding MF long-term plasticity in interneurons, focusing specifically on the induction and maintenance of LTP, and what the functional impact of persistent changes in efficacy at MF-interneuron synapses might be on the emergent properties of the inhibitory network dynamics in area CA3. This article is part of a Special Issue entitled 'Synaptic Plasticity & Interneurons'.

  • critical involvement of postsynaptic protein kinase activation in long term potentiation at Hippocampal Mossy Fiber synapses on ca3 interneurons
    The Journal of Neuroscience, 2010
    Co-Authors: Emilio J Galvan, Kathleen E Cosgrove, Jocelyn C Mauna, J P Card, Edda Thiels, Stephen D Meriney, German Barrionuevo
    Abstract:

    Hippocampal Mossy Fiber (MF) synapses on area CA3 lacunosum-moleculare (L-M) interneurons are capable of undergoing a Hebbian form of NMDA receptor (NMDAR)-independent long-term potentiation (LTP) induced by the same type of high-frequency stimulation (HFS) that induces LTP at MF synapses on pyramidal cells. LTP of MF input to L-M interneurons occurs only at synapses containing mostly calcium-impermeable (CI)-AMPA receptors (AMPARs). Here, we demonstrate that HFS-induced LTP at these MF-interneuron synapses requires postsynaptic activation of protein kinase A (PKA) and protein kinase C (PKC). Brief extracellular stimulation of PKA with forskolin (FSK) alone or in combination with 1-Methyl-3-isobutylxanthine (IBMX) induced a long-lasting synaptic enhancement at MF synapses predominantly containing CI-AMPARs. However, the FSK/IBMX-induced potentiation in cells loaded with the specific PKA inhibitor peptide PKI6-22 failed to be maintained. Consistent with these data, delivery of HFS to MFs synapsing onto L-M interneurons loaded with PKI6-22 induced posttetanic potentiation (PTP) but not LTP. Hippocampal sections stained for the catalytic subunit of PKA revealed abundant immunoreactivity in interneurons located in strata radiatum and L-M of area CA3. We also found that extracellular activation of PKC with phorbol 12,13-diacetate induced a pharmacological potentiation of the isolated CI-AMPAR component of the MF EPSP. However, HFS delivered to MF synapses on cells loaded with the PKC inhibitor chelerythrine exhibited PTP followed by a significant depression. Together, our data indicate that MF LTP in L-M interneurons at synapses containing primarily CI-AMPARs requires some of the same signaling cascades as does LTP of glutamatergic input to CA3 or CA1 pyramidal cells.

  • bidirectional hebbian plasticity at Hippocampal Mossy Fiber synapses on ca3 interneurons
    The Journal of Neuroscience, 2008
    Co-Authors: Emilio J Galvan, Eduardo Calixto, German Barrionuevo
    Abstract:

    Hippocampal area CA3 is critically involved in the formation of nonoverlapping neuronal subpopulations (“pattern separation”) to store memory representations as distinct events. Efficient pattern separation relies on the strong and sparse excitatory input from the Mossy Fibers (MFs) to pyramidal cells and feedforward inhibitory interneurons. However, MF synapses on CA3 pyramidal cells undergo long-term potentiation (LTP), which, if unopposed, will degrade pattern separation because MF activation will now recruit additional CA3 pyramidal cells. Here, we demonstrate MF LTP in stratum lacunosum-moleculare (L-M) interneurons induced by the same stimulation protocol that induces MF LTP in pyramidal cells. This LTP was NMDA receptor (NMDAR) independent and occurred at MF Ca2+-impermeable AMPA receptor synapses. LTP was prevented by with voltage clamping the postsynaptic cell soma during high-frequency stimulation (HFS), intracellular injections of the Ca2+ chelator BAPTA (20 mm), or bath applications of the L-type Ca2+ channel blocker nimodipine (10 μm). We propose that MF LTP in L-M interneurons preserves the sparsity of pyramidal cell activation, thus allowing CA3 to maintain its role in pattern separation. In the presence of the mGluR1α antagonist LY367385 \[( S )-(+)- a -amino-4-carboxy-2-methylbenzeneacetic acid\] (100 μm), the same HFS that induces MF LTP in naive slices triggered NMDAR-independent MF LTD. This LTD, like LTP, required activation of the L-type Ca2+ channel and also was induced after blockade of IP3 receptors with heparin (4 mg/ml) or the selective depletion of receptor-gated Ca2+ stores with ryanodine (10 or 100 μm). We conclude that L-M interneurons are endowed with Ca2+ signaling cascades suitable for controlling the polarity of MF long-term plasticity induced by joint presynaptic and postsynaptic activities.

  • giant miniature epscs at the Hippocampal Mossy Fiber to ca3 pyramidal cell synapse are monoquantal
    Journal of Neurophysiology, 2002
    Co-Authors: Darrell A. Henze, David B T Mcmahon, Kristen M Harris, German Barrionuevo
    Abstract:

    The mechanisms generating giant miniature excitatory postsynaptic currents (mEPSCs) were investigated at the Hippocampal Mossy Fiber (MF) to CA3 pyramidal cell synapse in vitro. These giant mEPSCs ...

  • Revisiting the role of the Hippocampal Mossy Fiber synapse.
    Hippocampus, 2001
    Co-Authors: Nathaniel N. Urban, Darrell A. Henze, German Barrionuevo
    Abstract:

    The Mossy Fiber pathway has long been considered to provide the major source of excitatory input to pyramidal cells of Hippocampal area CA3. In this review we describe anatomical and physiological properties of this pathway that challenge this view. We argue that the Mossy Fiber pathway does not provide the main input to CA3 pyramidal cells, and that the short-term plasticity and amplitude variance of Mossy Fiber synapses may be more important features than their long-term plasticity or absolute input strength.