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Cortico-Striatal Spike-Timing Dependent Plasticity After Activation of Subcortical Pathways

Cortico-striatal spike-timing dependent plasticity (STDP) is modulated by dopamine in vitro. The present study investigated STDP in vivo using alternative procedures for modulating dopaminergic inputs. Postsynaptic potentials (PSP) were evoked in intracellularly recorded spiny neurons by electrical...

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Autores principales: Schulz, Jan M., Redgrave, Peter, Reynolds, John N. J.
Formato: Texto
Lenguaje:English
Publicado: Frontiers Research Foundation 2010
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3059678/
https://www.ncbi.nlm.nih.gov/pubmed/21423509
http://dx.doi.org/10.3389/fnsyn.2010.00023
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author Schulz, Jan M.
Redgrave, Peter
Reynolds, John N. J.
author_facet Schulz, Jan M.
Redgrave, Peter
Reynolds, John N. J.
author_sort Schulz, Jan M.
collection PubMed
description Cortico-striatal spike-timing dependent plasticity (STDP) is modulated by dopamine in vitro. The present study investigated STDP in vivo using alternative procedures for modulating dopaminergic inputs. Postsynaptic potentials (PSP) were evoked in intracellularly recorded spiny neurons by electrical stimulation of the contralateral motor cortex. PSPs often consisted of up to three distinct components, likely representing distinct cortico-striatal pathways. After baseline recording, bicuculline (BIC) was ejected into the superior colliculus (SC) to disinhibit visual pathways to the dopamine cells and striatum. Repetitive cortical stimulation (∼60; 0.2 Hz) was then paired with postsynaptic spike discharge induced by an intracellular current pulse, with each pairing followed 250 ms later by a light flash to the contralateral eye (n = 13). Changes in PSPs, measured as the maximal slope normalized to 5-min pre, ranged from potentiation (∼120%) to depression (∼80%). The determining factor was the relative timing between PSP components and spike: PSP components coinciding or closely following the spike tended towards potentiation, whereas PSP components preceding the spike were depressed. Importantly, STDP was only seen in experiments with successful BIC-mediated disinhibition (n = 10). Cortico-striatal high-frequency stimulation (50 pulses at 100 Hz) followed 100 ms later by a light flash did not induce more robust synaptic plasticity (n = 9). However, an elevated post-light spike rate correlated with depression across plasticity protocols (R(2) = 0.55, p = 0.009, n = 11 active neurons). These results confirm that the direction of cortico-striatal plasticity is determined by the timing of pre- and postsynaptic activity and that synaptic modification is dependent on the activation of additional subcortical inputs.
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spelling pubmed-30596782011-03-21 Cortico-Striatal Spike-Timing Dependent Plasticity After Activation of Subcortical Pathways Schulz, Jan M. Redgrave, Peter Reynolds, John N. J. Front Synaptic Neurosci Neuroscience Cortico-striatal spike-timing dependent plasticity (STDP) is modulated by dopamine in vitro. The present study investigated STDP in vivo using alternative procedures for modulating dopaminergic inputs. Postsynaptic potentials (PSP) were evoked in intracellularly recorded spiny neurons by electrical stimulation of the contralateral motor cortex. PSPs often consisted of up to three distinct components, likely representing distinct cortico-striatal pathways. After baseline recording, bicuculline (BIC) was ejected into the superior colliculus (SC) to disinhibit visual pathways to the dopamine cells and striatum. Repetitive cortical stimulation (∼60; 0.2 Hz) was then paired with postsynaptic spike discharge induced by an intracellular current pulse, with each pairing followed 250 ms later by a light flash to the contralateral eye (n = 13). Changes in PSPs, measured as the maximal slope normalized to 5-min pre, ranged from potentiation (∼120%) to depression (∼80%). The determining factor was the relative timing between PSP components and spike: PSP components coinciding or closely following the spike tended towards potentiation, whereas PSP components preceding the spike were depressed. Importantly, STDP was only seen in experiments with successful BIC-mediated disinhibition (n = 10). Cortico-striatal high-frequency stimulation (50 pulses at 100 Hz) followed 100 ms later by a light flash did not induce more robust synaptic plasticity (n = 9). However, an elevated post-light spike rate correlated with depression across plasticity protocols (R(2) = 0.55, p = 0.009, n = 11 active neurons). These results confirm that the direction of cortico-striatal plasticity is determined by the timing of pre- and postsynaptic activity and that synaptic modification is dependent on the activation of additional subcortical inputs. Frontiers Research Foundation 2010-07-02 /pmc/articles/PMC3059678/ /pubmed/21423509 http://dx.doi.org/10.3389/fnsyn.2010.00023 Text en Copyright © 2010 Schulz, Redgrave and Reynolds. http://www.frontiersin.org/licenseagreement This is an open-access article subject to an exclusive license agreement between the authors and the Frontiers Research Foundation, which permits unrestricted use, distribution, and reproduction in any medium, provided the original authors and source are credited.
spellingShingle Neuroscience
Schulz, Jan M.
Redgrave, Peter
Reynolds, John N. J.
Cortico-Striatal Spike-Timing Dependent Plasticity After Activation of Subcortical Pathways
title Cortico-Striatal Spike-Timing Dependent Plasticity After Activation of Subcortical Pathways
title_full Cortico-Striatal Spike-Timing Dependent Plasticity After Activation of Subcortical Pathways
title_fullStr Cortico-Striatal Spike-Timing Dependent Plasticity After Activation of Subcortical Pathways
title_full_unstemmed Cortico-Striatal Spike-Timing Dependent Plasticity After Activation of Subcortical Pathways
title_short Cortico-Striatal Spike-Timing Dependent Plasticity After Activation of Subcortical Pathways
title_sort cortico-striatal spike-timing dependent plasticity after activation of subcortical pathways
topic Neuroscience
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3059678/
https://www.ncbi.nlm.nih.gov/pubmed/21423509
http://dx.doi.org/10.3389/fnsyn.2010.00023
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