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                <text>Mechanisms underlying enhancement of spontaneous glutamate release by group I mGluRs at a central auditory synapse</text>
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                <text>Journal Of Neuroscience</text>
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                <text>SYNAPTIC vesicles; auditory; mGluR; MNTB; EPSC; spontaneous glutamate release; voltage-gated sodium channel; DIRECTIONAL hearing; GLUTAMIC acid; MEMBRANE potential; SYNAPSES</text>
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                <text>Kang P;Wang X;Yuan W;Dainan L;Hai H;Yong L</text>
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                <text>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]</text>
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        <name>Kang P</name>
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        <name>Yong L</name>
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        <name>Yuan W</name>
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              <text>&lt;a href="http://doi.org/10.1166/jbn.2012.1361" target="_blank" rel="noreferrer noopener"&gt;http://doi.org/10.1166/jbn.2012.1361&lt;/a&gt;</text>
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              <text>161–171</text>
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                <text>Antitumor effect of novel gallium compounds and efficacy of nanoparticle-mediated gallium delivery in lung cancer.</text>
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                <text>Journal of biomedical nanotechnology</text>
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                <text>Antineoplastic Agents/*administration &amp; dosage/chemistry/pharmacokinetics; Biocompatible Materials/administration &amp; dosage/chemistry/pharmacokinetics; Cell Line; Cell Survival/drug effects; Coordination Complexes/*administration &amp; dosage/chemistry/pharmacokinetics; Drug Carriers/administration &amp; dosage/chemistry; Drug Stability; Endocytosis/drug effects; Gallium/*administration &amp; dosage/chemistry/pharmacokinetics; Hemolysis/drug effects; Humans; Lung Neoplasms/*drug therapy/metabolism; Materials Testing; Membrane Potential; Mitochondrial/drug effects; Nanoparticles/*administration &amp; dosage/chemistry; Particle Size; Platelet Aggregation/drug effects; Reactive Oxygen Species/metabolism; Transferrin/chemistry/pharmacology; Tumor</text>
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                <text>Wehrung Daniel; Oyewumi Moses O</text>
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                <text>The widespread application of gallium (Ga) in cancer therapy has been greatly hampered by lack of specificity resulting in poor tumor accumulation and retention. To address the challenge, two lipophilic gallium (III) compounds (gallium hexanedione; GaH and gallium acetylacetonate; GaAcAc) were synthesized and antitumor studies were conducted in human lung adenocarcinoma (A549) cells. Nanoparticles (NPs) containing various concentrations of the Ga compounds were prepared using a binary mixture of Gelucire 44/14 and cetyl alcohol as matrix materials. NPs were characterized based on size, morphology, stability and biocompatibility. Antitumor effects of free or NP-loaded Ga compounds were investigated based on cell viability, production of reactive oxygen species and reduction of mitochondrial potential. Compared to free Ga compounds, cytotoxicity of NP-loaded Ga (5-150 microg/ml) was less dependent on concentration and incubation time (exposure) with A549 cells. NP-mediated delivery (5-150 microg Ga/ml) enhanced antitumor effects of Ga compounds and the effect was pronounced at: (i) shorter incubation times; and (ii) at low concentrations of gallium (approximately 50 microg/ml) (p \textless 0.0006). Additional studies showed that</text>
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                <text>&lt;a href="http://doi.org/10.1166/jbn.2012.1361" target="_blank" rel="noreferrer noopener"&gt;10.1166/jbn.2012.1361&lt;/a&gt;</text>
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