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Coactivation of Pre- and Postsynaptic Signaling Mechanisms Determines Cell-Specific Spike-Timing-Dependent Plasticity

Synapses may undergo long-term increases or decreases in synaptic strength dependent on critical differences in the timing between pre-and postsynaptic activity. Such spike-timing-dependent plasticity (STDP) follows rules that govern how patterns of neural activity induce changes in synaptic strengt... Full description

Journal Title: Neuron 2007, Vol.54 (2), p.291-301
Main Author: Tzounopoulos, Thanos
Other Authors: Rubio, Maria E , Keen, John E , Trussell, Laurence O
Format: Electronic Article Electronic Article
Language: English
Subjects:
Quelle: Alma/SFX Local Collection
Publisher: United States: Elsevier Inc
ID: ISSN: 0896-6273
Link: https://www.ncbi.nlm.nih.gov/pubmed/17442249
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recordid: cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_2151977
title: Coactivation of Pre- and Postsynaptic Signaling Mechanisms Determines Cell-Specific Spike-Timing-Dependent Plasticity
format: Article
creator:
  • Tzounopoulos, Thanos
  • Rubio, Maria E
  • Keen, John E
  • Trussell, Laurence O
subjects:
  • Animals
  • Article
  • Calcium-Calmodulin-Dependent Protein Kinase Type 2
  • Calcium-Calmodulin-Dependent Protein Kinases - physiology
  • Cannabinoid Receptor Modulators - physiology
  • Cochlear Nucleus - cytology
  • Cochlear Nucleus - physiology
  • Cochlear Nucleus - ultrastructure
  • Electrophysiology
  • Excitatory Postsynaptic Potentials - physiology
  • Freeze Substitution
  • In Vitro Techniques
  • Learning - physiology
  • Long-Term Potentiation - physiology
  • Mice
  • Mice, Inbred ICR
  • Microscopy, Electron
  • MOLNEURO
  • musculoskeletal
  • Nerve Fibers - physiology
  • nervous system
  • neural
  • Neuronal Plasticity - physiology
  • Neuroscience(all)
  • ocular physiology
  • Receptor, Cannabinoid, CB1 - physiology
  • Receptors, Presynaptic - physiology
  • Receptors, Presynaptic - ultrastructure
  • Rodents
  • Signal Transduction - physiology
  • SIGNALING
  • Studies
  • Synaptic Transmission - physiology
  • Transmitters
ispartof: Neuron, 2007, Vol.54 (2), p.291-301
description: Synapses may undergo long-term increases or decreases in synaptic strength dependent on critical differences in the timing between pre-and postsynaptic activity. Such spike-timing-dependent plasticity (STDP) follows rules that govern how patterns of neural activity induce changes in synaptic strength. Synaptic plasticity in the dorsal cochlear nucleus (DCN) follows Hebbian and anti-Hebbian patterns in a cell-specific manner. Here we show that these opposing responses to synaptic activity result from differential expression of two signaling pathways. Ca2+/calmodulin-dependent protein kinase II (CaMKII) signaling underlies Hebbian postsynaptic LTP in principal cells. By contrast, in interneurons, a temporally precise anti-Hebbian synaptic spike-timing rule results from the combined effects of postsynaptic CaMKII–dependent LTP and endocannabinoid-dependent presynaptic LTD. Cell specificity in the circuit arises from selective targeting of presynaptic CB1 receptors in different axonal terminals. Hence, pre- and postsynaptic sites of expression determine both the sign and timing requirements of long-term plasticity in interneurons.
language: eng
source: Alma/SFX Local Collection
identifier: ISSN: 0896-6273
fulltext: fulltext
issn:
  • 0896-6273
  • 1097-4199
url: Link


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descriptionSynapses may undergo long-term increases or decreases in synaptic strength dependent on critical differences in the timing between pre-and postsynaptic activity. Such spike-timing-dependent plasticity (STDP) follows rules that govern how patterns of neural activity induce changes in synaptic strength. Synaptic plasticity in the dorsal cochlear nucleus (DCN) follows Hebbian and anti-Hebbian patterns in a cell-specific manner. Here we show that these opposing responses to synaptic activity result from differential expression of two signaling pathways. Ca2+/calmodulin-dependent protein kinase II (CaMKII) signaling underlies Hebbian postsynaptic LTP in principal cells. By contrast, in interneurons, a temporally precise anti-Hebbian synaptic spike-timing rule results from the combined effects of postsynaptic CaMKII–dependent LTP and endocannabinoid-dependent presynaptic LTD. Cell specificity in the circuit arises from selective targeting of presynaptic CB1 receptors in different axonal terminals. Hence, pre- and postsynaptic sites of expression determine both the sign and timing requirements of long-term plasticity in interneurons.
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subjectAnimals ; Article ; Calcium-Calmodulin-Dependent Protein Kinase Type 2 ; Calcium-Calmodulin-Dependent Protein Kinases - physiology ; Cannabinoid Receptor Modulators - physiology ; Cochlear Nucleus - cytology ; Cochlear Nucleus - physiology ; Cochlear Nucleus - ultrastructure ; Electrophysiology ; Excitatory Postsynaptic Potentials - physiology ; Freeze Substitution ; In Vitro Techniques ; Learning - physiology ; Long-Term Potentiation - physiology ; Mice ; Mice, Inbred ICR ; Microscopy, Electron ; MOLNEURO ; musculoskeletal ; Nerve Fibers - physiology ; nervous system ; neural ; Neuronal Plasticity - physiology ; Neuroscience(all) ; ocular physiology ; Receptor, Cannabinoid, CB1 - physiology ; Receptors, Presynaptic - physiology ; Receptors, Presynaptic - ultrastructure ; Rodents ; Signal Transduction - physiology ; SIGNALING ; Studies ; Synaptic Transmission - physiology ; Transmitters
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abstractSynapses may undergo long-term increases or decreases in synaptic strength dependent on critical differences in the timing between pre-and postsynaptic activity. Such spike-timing-dependent plasticity (STDP) follows rules that govern how patterns of neural activity induce changes in synaptic strength. Synaptic plasticity in the dorsal cochlear nucleus (DCN) follows Hebbian and anti-Hebbian patterns in a cell-specific manner. Here we show that these opposing responses to synaptic activity result from differential expression of two signaling pathways. Ca2+/calmodulin-dependent protein kinase II (CaMKII) signaling underlies Hebbian postsynaptic LTP in principal cells. By contrast, in interneurons, a temporally precise anti-Hebbian synaptic spike-timing rule results from the combined effects of postsynaptic CaMKII–dependent LTP and endocannabinoid-dependent presynaptic LTD. Cell specificity in the circuit arises from selective targeting of presynaptic CB1 receptors in different axonal terminals. Hence, pre- and postsynaptic sites of expression determine both the sign and timing requirements of long-term plasticity in interneurons.
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