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SH3 fusion protein pull downs using ITSN1SH3 A reveal diurnally varying binding of VGLUT1 with slightly reduced VGLUT1/dynamin ratios at the beginning of the light (ZT 0) or the dark (ZT 12) period. Phosphorylation increases binding of VGLUT1 but not of dynamin to EnphSH3. In contrast binding of dynamin to ITSN1SH3 A decreases under phosphorylating conditions with no changes in VGLUT1 binding.
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Study shows by live-cell imaging with pH- and chloride-sensitive fluorescent probes in cultured hippocampal neurons of wild-type and VGLUT1-deficient mice that in synaptic vesicles VGLUT functions as a glutamate/proton exchanger associated with a channel-like chloride conductance.
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early VGLUT1-specific parallel fiber synaptic input deficits and dysregulated cerebellar circuit as potential mediators of cerebellar dysfunction in frataxin knock-in/knockout mice.
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Mice heterozygous for the vesicular glutamate transporter 1 (VGLUT1+/-) were used. Firstly, mRNA expression of the different members of the HDAC superfamily in the prefrontal cortex (PFC) of VGLUT1+/- mice and WT littermates were studied by RT-PCR.
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These findings suggest that nitrosylation of VAChT and VGLUT1 may be associated with dysfunctional acetylcholinergic and glutamatergic neurotransmission in Alzheimer's disease.
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Study revealed susceptibility of glutamatergic nerve terminals to Abeta induced toxicity and underlined the importance of VGLUT1 in the progression of Alzheimer's disease, as the decrease of this protein levels could increase the susceptibility to subsequent deleterious inputs by exacerbating Abeta induced neuroinflammation and synaptic plasticity disruption.
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triple KO of Slc17a7, Slc17a6, and Slc17a8 diminished IIIS, which was rescued by exogenously introduced wild-type Slc17a7 or Slc17a6 genes
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The observed changes in gene and protein expression of vesicular transporter 2, regional architecture, and morphology of mouse auditory forebrain may relate to-and to some extent enable-the emergence of mature sound-evoked activity patterns.
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In CA1 pyramidal neurons, a slow excitatory postsynaptic current is absent in the VGLUT1 knockout mouse.
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Data show that activation of nucleotide receptor P2Y4 (P2Y4) in the differentiating embryonic stem cells (ESCs) resulted in an increased proportion of neurons expressing vesicular glutamate transporter (vGluT).
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Results suggest that activation of JNK in Alzheimer's disease (AD) inhibits insulin signaling which could lead to a decreased expression of VGLUT1, therefore contributing to the glutamatergic deficit in AD
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Distribution of VGLUT1 and VGLUT2 in the CN, previously described for guinea pig, was replicated in mouse and showed similar changes in VGLUT1 and 2 distributions after unilateral cochlear insult
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Here, we show that VGluT1(+/-) mice acquired the initial visual discrimination at the same rate as controls. However, they failed to suppress responses to the previously rewarded stimulus following reversal of reward contingencies.
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conclude that VGLUTs contain two anion binding sites and one cation binding site, allowing the transporter to adjust to the changing ionic conditions during vesicle filling without being dependent on other transporters or channels.
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our genetic analysis provides new in vivo evidence that VGluT1(+) glutamatergic signaling, mediated by the astroglial mGluR5 receptor, regulates the functional maturation of cortical astroglia during development.
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Targeting of VGLUT-1 in the hippocampus leads to cognitive deficits in a knocked-down adult mouse model.
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VGLUT1 enhances the tonicity of excitatory synaptic vesicles and stabilises SVs at presynaptic terminals.
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This study demonstrates a key role for VGLUT1 in long-loop glutamatergic feedback control of 5-HT function.
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These data indicate that VGluT1, but not VGluT2, plays a role in the neural processes underlying inhibitory learning
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This study demonistrated that Increased expression of the Vesicular Glutamate Transporter-1 (VGLUT1) in the prefrontal cortex after Antidepressant Drugs treatment in mice.
