1
40
3
-
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/" 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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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
A name given to the resource
Mechanisms underlying enhancement of spontaneous glutamate release by group I mGluRs at a central auditory synapse
Publisher
An entity responsible for making the resource available
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]
Identifier
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<a href="http://doi.org/" target="_blank" rel="noreferrer noopener"></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).
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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
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/10.1016/0014-2999(92)90390-p" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/0014-2999(92)90390-p</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
337-341
Issue
3
Volume
211
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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
A name given to the resource
The Actions Of 3-aminopropanephosphinic Acid At Gaba(b) Receptors In Rat Hippocampus
Publisher
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European Journal of Pharmacology
Date
A point or period of time associated with an event in the lifecycle of the resource
1992
1992-02
Subject
The topic of the resource
2-hydroxy-saclofen; b receptors; baclofen; brain slices; ca3 pyramidal cells; excitatory transmission; gaba(b) receptors (postsynaptic); gaba(b) receptors (presynaptic); inhibitory transmission; in-vitro; neurons; patch; Pharmacology & Pharmacy; potent; slice recording; synapses; transmission
Creator
An entity primarily responsible for making the resource
Lovinger D M; Harrison N L; Lambert N A
Identifier
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<a href="http://doi.org/10.1016/0014-2999(92)90390-p" target="_blank" rel="noreferrer noopener">10.1016/0014-2999(92)90390-p</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
1992
2-hydroxy-saclofen
b receptors
baclofen
brain slices
ca3 pyramidal cells
European journal of pharmacology
excitatory transmission
gaba(b) receptors (postsynaptic)
gaba(b) receptors (presynaptic)
Harrison N L
in-vitro
inhibitory transmission
Lambert N A
Lovinger D M
Neurons
patch
Pharmacology & Pharmacy
potent
slice recording
synapses
Transmission
-
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/10.1111/j.1471-4159.2004.02834.x" target="_blank" rel="noreferrer noopener">http://doi.org/10.1111/j.1471-4159.2004.02834.x</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
59-71
Issue
1
Volume
92
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Title
A name given to the resource
RNAi knockdown of Par-4 inhibits neurosynaptic degeneration in ALS-linked mice
Publisher
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Journal of Neurochemistry
Date
A point or period of time associated with an event in the lifecycle of the resource
2005
2005-01
Subject
The topic of the resource
amyotrophic lateral sclerosis; amyotrophic lateral sclerosis; anterior horn; antisense oligonucleotides; apoptosis; apoptosis response-4; Biochemistry & Molecular Biology; cells; Cu/Zn superoxide dismutase; motor-neuron degeneration; neurons; Neurosciences & Neurology; prostate; protein; RNA interference; sod1; spinal motor neurons; synapse; synapses; transgenic mouse model
Creator
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Xie J; Awad K S; Guo Q
Description
An account of the resource
Evidence from human amyotrophic lateral sclerosis (ALS) patients and ALS-linked Cu/Zn superoxide dismutase (Cu/Zn-SOD) transgenic mice bearing the mutation of glycine to alanine at position 93 (G93A) suggests that the pro-apoptotic protein prostate apoptosis response-4 (Par-4) might be a critical link in the chain of events leading to motor neuron degeneration. We now report that Par-4 is enriched in synaptosomes and post-synaptic density from the ventral horn of the spinal cord. Levels of Par-4 in synaptic compartments increased significantly during rapid and slow declining stages of muscle strength in hSOD1 G93A mutant mice. In the pre-muscle weakness stage, hSOD1 G93A mutation sensitized synaptosomes from the ventral horn of the spinal cord to increased levels of Par-4 expression following excitotoxic and apoptotic insults. In ventral spinal synaptosomes, Par-4-mediated production of pro-apoptotic cytosolic factor(s) was significantly enhanced by the hSOD1 G93A mutation. RNA interference (RNAi) knockdown of Par-4 inhibited mitochondrial dysfunction and caspase-3 activation induced by G93A mutation in synaptosomes from the ventral horn of the spinal cord, and protected spinal motor neurons from apoptosis. These results identify the synapse as a crucial cellular site for the cell death promoting actions of Par-4 in motor neurons, and suggest that targeted inhibition of Par-4 by RNAi may prove to be a neuroprotective strategy for motor neuron degeneration.
Identifier
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<a href="http://doi.org/10.1111/j.1471-4159.2004.02834.x" target="_blank" rel="noreferrer noopener">10.1111/j.1471-4159.2004.02834.x</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article
2005
amyotrophic lateral sclerosis
anterior horn
antisense oligonucleotides
Apoptosis
apoptosis response-4
Awad K S
Biochemistry & Molecular Biology
Cells
Cu/Zn superoxide dismutase
Guo Q
Journal Article
Journal of neurochemistry
motor-neuron degeneration
Neurons
Neurosciences & Neurology
Prostate
Protein
RNA Interference
sod1
spinal motor neurons
synapse
synapses
transgenic mouse model
Xie J