Synergistic Release of Ca2+ from IP3-Sensitive Stores Evoked by Synaptic Activation of mGluRs Paired with Backpropagating Action Potentials

Nakamura, Takeshi; Barbara, Jean-Gaël; Nakamura, Kyoko; Ross, William N.

doi:10.1016/s0896-6273(00)81125-3

Cited by 312 publications

(441 citation statements)

References 54 publications

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“…With extracellular stimulation of Schaffer collaterals (100 Hz; four pulses; 20 -50 A; 100 s duration), mGluR-mediated EPSCs were consistently evoked in CA1 pyramidal cells, as previously reported (Congar et al, 1997;Nakamura et al, 1999). A metabotropic response was, however, only observed with highresistance recording pipettes (n ϭ 10 and 28 for low-and highresistance pipettes, respectively) (Fig.…”

Section: A Single Ca3 Pyramidal Cell Does Not Induce Mglur-ltd In a Csupporting

confidence: 84%

Activation Conditions for the Induction of Metabotropic Glutamate Receptor-Dependent Long-Term Depression in Hippocampal CA1 Pyramidal Cells

Fan¹,

Ster²,

Gerber³

2010

J. Neurosci.

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Two forms of homosynaptic long-term depression (LTD) are distinguished in hippocampal CA1 pyramidal cells, one which is NMDA receptor dependent and the other metabotropic glutamate receptor (mGluR) dependent. Although the molecular processes involved in mGluR-LTD are well characterized, the conditions of circuit activation required for its induction remain unclear. We show that mGluR-LTD cannot be induced in synaptically coupled CA3-CA1 pyramidal cell pairs. Experiments to address the underlying mechanisms indicate that, even when glutamate transporters are blocked, one presynaptic cell releases insufficient glutamate to evoke an mGluRmediated current in a connected CA1 cell. These findings imply that extrasynaptic diffusion is not a limiting factor and are consistent with a sparse distribution of functional mGluRs in the dendritic tree of pyramidal cells. Thus, the discharge of multiple Schaffer collaterals to a targeted cell is necessary for mGluR-LTD. Our experiments indicate that approximately eight CA3 inputs to a CA1 pyramidal cell must be activated to induce mGluR-LTD.

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Section: A Single Ca3 Pyramidal Cell Does Not Induce Mglur-ltd In a Csupporting

confidence: 84%

Activation Conditions for the Induction of Metabotropic Glutamate Receptor-Dependent Long-Term Depression in Hippocampal CA1 Pyramidal Cells

Fan¹,

Ster²,

Gerber³

2010

J. Neurosci.

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“…LTP has generally not been observed at synapses between parallel fibers and Purkinje cells. Purkinje cells require the synergistic action of mGluRs and a rise in IP 3 to release Ca 2ϩ from intracellular stores with voltage-sensitive Ca 2ϩ channels for the induction of LTD (39)(40)(41). In the absence of mGluR1 or of IP 3 receptors, LTD is not observed in Purkinje cells and motor coordination is abnormal (42)(43)(44).…”

Section: Discussionmentioning

confidence: 99%

Bidirectional synaptic plasticity in the cerebellum-like mammalian dorsal cochlear nucleus

Fujino

Oertel

2002

Proc. Natl. Acad. Sci. U.S.A.

116

133

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The dorsal cochlear nucleus integrates acoustic with multimodal sensory inputs from widespread areas of the brain. Multimodal inputs are brought to spiny dendrites of fusiform and cartwheel cells in the molecular layer by parallel fibers through synapses that are subject to long-term potentiation and long-term depression. Acoustic cues are brought to smooth dendrites of fusiform cells in the deep layer by auditory nerve fibers through synapses that do not show plasticity. Plasticity requires Ca 2؉ -induced Ca 2؉ release; its sensitivity to antagonists of N-methyl-D-aspartate and metabotropic glutamate receptors differs in fusiform and cartwheel cells.A uditory nerve fibers bring acoustic information to the cochlear nucleus and feed it into several parallel pathways that ascend through the brainstem. Pathways through the dorsal cochlear nucleus (DCN) are thought to detect spectral cues for localizing sounds monaurally (1). Those through the ventral cochlear nucleus (VCN) encode spectral and temporal characteristics that allow sounds to be localized in the horizontal plane, through binaural circuits, and recognized.The DCN resembles the cerebellum, cartwheel cells being homologues of cerebellar Purkinje cells (2). Fusiform cells project to the inferior colliculus. Granule cells in the vicinity of the cochlear nuclei are innervated by diverse regions of the brain, including the dorsal column nuclei (1), vestibular periphery (3), and auditory nuclei (4, 5). Their unmyelinated axons, parallel fibers, contact spiny dendrites of fusiform and cartwheel cells. Myelinated auditory nerve fibers contact smooth basal dendrites of fusiform cells. The DCN resembles the electrosensory lobes in fishes even more closely (6, 7).In cerebellar circuits, the gain of one of two converging systems of inputs varies as a function of activity. Long-term depression (LTD) at parallel fiber synapses in cerebellar Purkinje cells evoked by coincident excitation through parallel fiber and climbing fiber synapses plays a role in coordination and motor learning (8). Long-term potentiation (LTP) and LTD at parallel fiber synapses are evoked in electric fishes by convergent excitation by parallel fibers and sensory afferents to compensate for an animal's own signals in localizing external sources (9). We show that principal cells of the DCN combine multimodal inputs through parallel fibers whose strength is modulated by activity with invariant acoustic input through auditory nerve fibers. MethodsCoronal slices (200 m) containing the DCN were prepared from ICR mice (Harlan-Sprague-Dawley) between 18 and 20 days old with an oscillating tissue slicer (VT1000S, Leica Microsystems, Nussloch, Germany). Slices were held in a 300-l chamber that was superfused at 3-5 ml͞min with oxygenated saline at Ϸ33°C. Experiments were done in accordance with the protocols and guidelines of the Animal Care and Use Committee at the University of Wisconsin, Madison.Whole-cell patch-clamp recordings were generally made with 3-to 5-M⍀ pipettes filled with a K-gluconate-base...

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“…Back-propagating dendritic action potentials are likely to play an important role in triggering the increases in intracellular calcium necessary for DSI in these conditions (Morishita & Alger, 2001). Combining backpropagating action potentials with synaptic activation of mGluRs (Nakamura et al, 1999) was shown to induce increases in intracellular calcium in the micromolar range, thus well in the order of magnitude shown by Wang & Zucker (2000) to be required for DSI induction.…”

Section: Physiological Induction Protocols Of Hippocampal Dsimentioning

confidence: 95%

Endocannabinoid‐mediated short‐term synaptic plasticity: depolarization‐induced suppression of inhibition (DSI) and depolarization‐induced suppression of excitation (DSE)

Diana

Marty

2004

British J Pharmacology

238

177

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Depolarization-induced suppression of inhibition (DSI) and depolarization-induced suppression of excitation (DSE) are two related forms of short-term synaptic plasticity of GABAergic and glutamatergic transmission, respectively. They are induced by calcium concentration increases in postsynaptic cells and are mediated by the release of a retrograde messenger, which reversibly inhibits afferent synapses via presynaptic mechanisms. We review here:(1) The evidence accumulated during the 1990s that has led to the conclusion that DSI/DSE rely on retrograde signaling. (2) The more recent research that has led to the identification of endocannabinoids as the retrograde messengers responsible for DSI/DSE. (3) The possible mechanisms by which presynaptic type 1 cannabinoid receptors reduce synaptic efficacy during DSI/DSE. (4) The possible modes of induction of DSI/DSE by physiological activity patterns, and the partially conflicting evaluations of the calcium concentration increases required for cannabinoid synthesis. (5) Finally, the relation between DSI/DSE and other forms of long-and short-term synaptic inhibition, which were more recently associated with the production of endocannabinoids by postsynaptic cells.We conclude that recent studies on DSI/DSE have uncovered a specific and original mode of action for endocannabinoids in the brain, and that they have opened new avenues to understand the role of retrograde signaling in central synapses.

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Synergistic Release of Ca2+ from IP3-Sensitive Stores Evoked by Synaptic Activation of mGluRs Paired with Backpropagating Action Potentials

Cited by 312 publications

References 54 publications

Activation Conditions for the Induction of Metabotropic Glutamate Receptor-Dependent Long-Term Depression in Hippocampal CA1 Pyramidal Cells

Activation Conditions for the Induction of Metabotropic Glutamate Receptor-Dependent Long-Term Depression in Hippocampal CA1 Pyramidal Cells

Bidirectional synaptic plasticity in the cerebellum-like mammalian dorsal cochlear nucleus

Endocannabinoid‐mediated short‐term synaptic plasticity: depolarization‐induced suppression of inhibition (DSI) and depolarization‐induced suppression of excitation (DSE)

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