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Text
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URL Address
<a href="http://doi.org/10.1016/j.neuroscience.2016.03.010" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.neuroscience.2016.03.010</a>
Pages
177–190
Volume
324
Dublin Core
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Title
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Intrinsic plasticity induced by group II metabotropic glutamate receptors via enhancement of high-threshold KV currents in sound localizing neurons.
Publisher
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Neuroscience
Date
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2016
2016-06
Subject
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Acoustic Stimulation/methods; Action Potentials/drug effects/physiology; Animals; Auditory Pathways/drug effects/*physiology; Brain/drug effects/physiology; Chick Embryo; Glutamic Acid/metabolism; metabotropic glutamate receptor; Metabotropic Glutamate/agonists/*metabolism; neuromodulation; Neuronal Plasticity/drug effects/*physiology; Neurons/drug effects/*physiology; nucleus laminaris; Patch-Clamp Techniques; Potassium Channels; Potassium/metabolism; Protein Kinase C/metabolism; Receptors; Sound Localization/drug effects/*physiology; Tissue Culture Techniques; Type C Phospholipases/metabolism; voltage-gated potassium channel; Voltage-Gated/*metabolism
Creator
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Hamlet W R; Lu Y
Description
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Intrinsic plasticity has emerged as an important mechanism regulating neuronal excitability and output under physiological and pathological conditions. Here, we report a novel form of intrinsic plasticity. Using perforated patch clamp recordings, we examined the modulatory effects of group II metabotropic glutamate receptors (mGluR II) on voltage-gated potassium (KV) currents and the firing properties of neurons in the chicken nucleus laminaris (NL), the first central auditory station where interaural time cues are analyzed for sound localization. We found that activation of mGluR II by synthetic agonists resulted in a selective increase of the high-threshold KV currents. More importantly, synaptically released glutamate (with reuptake blocked) also enhanced the high-threshold KV currents. The enhancement was frequency-coding region dependent, being more pronounced in low-frequency neurons compared to middle- and high-frequency neurons. The intracellular mechanism involved the Gbetagamma signaling pathway associated with phospholipase C and protein kinase C. The modulation strengthened membrane outward rectification, sharpened action potentials, and improved the ability of NL neurons to follow high-frequency inputs. These data suggest that mGluR II provides a feedforward modulatory mechanism that may regulate temporal processing under the condition of heightened synaptic inputs.
Identifier
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<a href="http://doi.org/10.1016/j.neuroscience.2016.03.010" target="_blank" rel="noreferrer noopener">10.1016/j.neuroscience.2016.03.010</a>
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2016
Acoustic Stimulation/methods
Action Potentials/drug effects/physiology
Animals
Auditory Pathways/drug effects/*physiology
Brain/drug effects/physiology
Chick Embryo
Department of Anatomy & Neurobiology
Glutamic Acid/metabolism
Hamlet W R
Lu Y
metabotropic glutamate receptor
Metabotropic Glutamate/agonists/*metabolism
NEOMED College of Medicine
neuromodulation
Neuronal Plasticity/drug effects/*physiology
Neurons/drug effects/*physiology
Neuroscience
nucleus laminaris
Patch-Clamp Techniques
Potassium Channels
Potassium/metabolism
Protein Kinase C/metabolism
Receptors
Sound Localization/drug effects/*physiology
Tissue Culture Techniques
Type C Phospholipases/metabolism
voltage-gated potassium channel
Voltage-Gated/*metabolism