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40
4
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Text
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URL Address
<a href="http://doi.org/" target="_blank" rel="noreferrer noopener">http://doi.org/</a>
Pages
7027-7042
Issue
37
Volume
40
ISSN
2706474
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September 2020 List
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NEOMED College of Medicine Postdoc
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NEOMED Postdoc Publications
Dublin Core
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Title
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Mechanisms underlying enhancement of spontaneous glutamate release by group I mGluRs at a central auditory synapse
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Journal Of Neuroscience
Date
A point or period of time associated with an event in the lifecycle of the resource
2020
2020-09-09
Subject
The topic of the resource
SYNAPTIC vesicles; auditory; mGluR; MNTB; EPSC; spontaneous glutamate release; voltage-gated sodium channel; DIRECTIONAL hearing; GLUTAMIC acid; MEMBRANE potential; SYNAPSES
Creator
An entity primarily responsible for making the resource
Kang P;Wang X;Yuan W;Dainan L;Hai H;Yong L
Description
An account of the resource
One emerging concept in neuroscience states that synaptic vesicles and the molecular machinery underlying spontaneous transmitter release are different from those underlying action potential-driven synchronized transmitter release. Differential neuromodulation of these two distinct release modes by metabotropic glutamate receptors (mGluRs) constitutes critical supporting evidence. However, the mechanisms underlying such a differential modulation are not understood. Here, we investigated the mechanisms of the modulation by group I mGluRs (mGluR I) on spontaneous glutamate release in the medial nucleus of the trapezoid body (MNTB), an auditory brainstem nucleus critically involved in sound localization. Whole-cell patch recordings from brainstem slices of mice of both sexes were performed. Activation of mGluR I by 3,5-DHPG (200 μM) produced an inward current at -60 mV, and increased spontaneous glutamate release in MNTB neurons. Pharmacological evidence indicated involvement of both mGluR1 and mGluR5, which was further supported for mGluR5 by immunolabeling results. The modulation was eliminated by blocking NaV channels (tetrodotoxin, 1 μM), persistent Na+ current (INaP) (Riluzole, 10 μM), or CaV channels (CdCl2, 100 µM). Presynaptic calyx recordings revealed that 3,5-DHPG shifted the activation of INaP to more hyperpolarized voltages and increased INaP at resting membrane potential. Our data indicate that mGluR I enhance spontaneous glutamate release via regulation of INaP and subsequent Ca2+-dependent processes under rest condition. [ABSTRACT FROM AUTHOR]
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<a href="http://doi.org/" target="_blank" rel="noreferrer noopener"></a>
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journalArticle
2020
Auditory
Dainan L
directional hearing
EPSC
Glutamic Acid
Hai H
Journal of Neuroscience
journalArticle
Kang P
Membrane Potential
mGluR
MNTB
NEOMED College of Medicine Postdoc
NEOMED Postdoc Publications
September 2020 List
spontaneous glutamate release
synapses
SYNAPTIC vesicles
voltage-gated sodium channel
Wang X
Yong L
Yuan W
-
Text
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URL Address
<a href="http://doi.org/10.1016/j.brainres.2019.04.006" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.brainres.2019.04.006</a>
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
95-103
Volume
1717
Dublin Core
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Title
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Subtle differences in synaptic transmission in medial nucleus of trapezoid body neurons between wild-type and Fmr1 knockout mice
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Brain Research
Date
A point or period of time associated with an event in the lifecycle of the resource
2019
2019-08
Subject
The topic of the resource
Fragile X syndrome; MNTB; Synaptic excitation; Synaptic inhibition
Creator
An entity primarily responsible for making the resource
Lu Yong
Description
An account of the resource
In animal models for fragile X syndrome where the gene for fragile X mental retardation protein is knocked out (Fmr1 KO), neurotransmission in multiple brain regions shifts excitation/inhibition balance, resulting in hyperexcitability in neural circuits. Here, using whole-cell recordings from brainstem slices, we investigated synaptic transmission at the medial nucleus of trapezoid body (MNTB, a critical nucleus in the brainstem sound localization circuit), in Fmr1 KO and wild-type (WT) mice 2-3 weeks of age in both sexes. Surprisingly, neither synaptic excitation nor inhibition in KO neurons was significantly changed. The synaptic strength, kinetics, and short-term plasticity of synaptic excitation remained largely unaltered. Subtle differences were observed in response patterns, with KO neurons displaying less all-or-none eEPSCs. Similarly, synaptic inhibition mediated by glycine and GABA remains largely unchanged, except for a slower kinetics of mixed sIPSCs. In pharmacologically isolated glycinergic and GABAergic inhibition, no significant differences in synaptic strength and kinetics were detected between the two genotypes. These results demonstrate that at the cellular level synaptic transmission at MNTB is largely unaffected in Fmr1 KO mice by 2-3 weeks after birth, suggesting the existence of compensatory mechanisms that maintain the inhibitory output of MNTB to its targets in the auditory brainstem.
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<a href="http://doi.org/10.1016/j.brainres.2019.04.006" target="_blank" rel="noreferrer noopener">10.1016/j.brainres.2019.04.006</a>
2019
Brain research
Department of Anatomy & Neurobiology
Fragile X syndrome
June 2019 Update
Lu Yong
MNTB
NEOMED College of Medicine
Synaptic excitation
synaptic inhibition
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1523/JNEUROSCI.0603-18.2018" target="_blank" rel="noreferrer noopener">http://doi.org/10.1523/JNEUROSCI.0603-18.2018</a>
Pages
8187–8199
Issue
38
Volume
38
Dublin Core
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Title
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Neurotransmitter- and Release-Mode-Specific Modulation of Inhibitory Transmission by Group I Metabotropic Glutamate Receptors in Central Auditory Neurons of the Mouse.
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The Journal of neuroscience : the official journal of the Society for Neuroscience
Date
A point or period of time associated with an event in the lifecycle of the resource
2018
2018-09
Subject
The topic of the resource
GABA; glycine; IPSC; mGluR; MNTB; neuromodulation
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Curry Rebecca J; Peng Kang; Lu Yong
Description
An account of the resource
Neuromodulation mediated by metabotropic glutamate receptors (mGluRs) regulates many brain functions. However, the functions of mGluRs in the auditory system under normal and diseased states are not well understood. The medial nucleus of the trapezoid body (MNTB) is a critical nucleus in the auditory brainstem nuclei involved in sound localization. In addition to the classical calyx excitatory inputs, MNTB neurons also receive synaptic inhibition and it remains entirely unknown how this inhibition is regulated. Here, using whole-cell voltage clamp in brain slices, we investigated group I mGluR (mGluR I)-mediated modulation of the glycinergic and GABAergic inputs to MNTB neurons in both WT mice and a fragile X syndrome (FXS) mouse model (both sexes) in which the fragile X mental retardation gene 1 is knocked out (Fmr1 KO), causing exaggerated activity of mGluR I and behavioral phenotypes. Activation of mGluR I by (RS)-3,5-dihydroxyphenylglycine (3,5-DHPG) increased the frequency and amplitude of glycinergic spontaneous IPSCs (sIPSCs) in both WT and Fmr1 KO neurons in a voltage-gated sodium channel-dependent fashion, but did not modulate glycinergic evoked IPSCs (eIPSCs). In contrast, 3,5-DHPG did not affect GABAergic sIPSCs, but did suppress eIPSCs in WT neurons via endocannabinoid signaling. In the KO, the effect of 3,5-DHPG on GABAergic eIPSCs was highly variable, which supports the notion of impaired GABAergic signaling in the FXS model. The differential modulation of sIPSC and eIPSC and differential modulation of glycinergic and GABAergic transmission suggest distinct mechanisms responsible for spontaneous and evoked release of inhibitory transmitters and their modulation through the mGluR I signaling pathway.SIGNIFICANCE STATEMENT Neurons communicate with each other through the release of neurotransmitters, which assumes two basic modes, spontaneous and evoked release. These two release modes are believed to function using the same vesicle pool and machinery. Recent works have challenged this dogma, pointing to distinct vesicle release mechanisms underlying the two release modes. Here, we provide the first evidence in the central auditory system supporting this novel concept. We discovered neural-transmitter- and release-mode-specific neuromodulation of inhibitory transmission by metabotropic glutamate receptors and revealed part of the signaling pathways underlying this differential modulation. The results establish the foundation for a multitude of directions to study physiological significance of different release modes in auditory processing.
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<a href="http://doi.org/10.1523/JNEUROSCI.0603-18.2018" target="_blank" rel="noreferrer noopener">10.1523/JNEUROSCI.0603-18.2018</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).
2018
Curry Rebecca J
Department of Anatomy & Neurobiology
GABA
glycine
IPSC
Lu Yong
mGluR
MNTB
NEOMED College of Medicine
neuromodulation
Peng Kang
The Journal of neuroscience : the official journal of the Society for Neuroscience
-
Text
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URL Address
<a href="http://doi.org/10.1016/j.neulet.2013.11.051" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.neulet.2013.11.051</a>
Pages
152–157
Volume
559
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
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Postnatal developmental changes in the medial nucleus of the trapezoid body in a mouse model of auditory pathology.
Publisher
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Neuroscience letters
Date
A point or period of time associated with an event in the lifecycle of the resource
2014
2014-01
Subject
The topic of the resource
*Disease Models; AHL; Animal; Animals; Auditory brainstem responses; Auditory Pathways/*growth & development/*pathology; Auditory system; DBA/2; Hearing Loss/*pathology; Inbred CBA; Inbred DBA; Mice; MNTB; Newborn; Olivary Nucleus/*growth & development/*pathology; Organ Culture Techniques
Creator
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Grimsley Calum A; Sivaramakrishnan Shobhana
Description
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Age-related hearing loss (AHL) is a multifactorial disorder characterized by a decline in peripheral and central auditory function. Here, we examined synaptic transmission in DBA/2 mice, which carry the AHL8 gene, at the identifiable glutamatergic synapse in the medial nucleus of the trapezoid body (MNTB), a nucleus in the superior olivary complex critical for acoustic timing. Mice exhibited raised auditory brainstem thresholds by P14, soon after hearing onset. Excitatory postsynaptic currents were prolonged; however, postsynaptic excitability was normal. By P18, high-frequency hearing loss was evident. Coincident with the onset of hearing loss, MNTB principal neurons displayed changes in intrinsic firing properties. These results suggest that changes in transmission in the superior olivary complex are associated with early onset hearing loss.
Identifier
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<a href="http://doi.org/10.1016/j.neulet.2013.11.051" target="_blank" rel="noreferrer noopener">10.1016/j.neulet.2013.11.051</a>
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Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*Disease Models
2014
AHL
Animal
Animals
Auditory brainstem responses
Auditory Pathways/*growth & development/*pathology
Auditory system
DBA/2
Grimsley Calum A
Hearing Loss/*pathology
Inbred CBA
Inbred DBA
Mice
MNTB
Neuroscience letters
Newborn
Olivary Nucleus/*growth & development/*pathology
Organ Culture Techniques
Sivaramakrishnan Shobhana