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Aged VAChT-deficient mice showed a decrease in the number of hippocampal neurons and Alzheimer's-Like Pathology.
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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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Studied object recognition and spatial location in mice deficient for Vesicular Acetylcholine Transporter (VAChT) within interneurons of the striatum, found: impairment in home cage object recognition with a 15 min retention delay, but not with a 3 h retention delay; no on memory for the location of objects; sex differences in retention
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VAChT overexpression increases acetylcholine at the synaptic cleft and accelerates aging of neuromuscular junctions. Data demonstrate that increasing levels of acetylcholine at the synaptic cleft promote degeneration of adult neuromuscular junction, contributing to age- and disease-related motor deficits.
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Old VAChT deficient mice (13-16 months-old) showed more pronounced motor learning/balance deficits on the rotarod, and more pronounced balance deficits on the catwalk
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These results suggest that the VAChT-Cre lines are Cre-drivers that have selectivity in S and FR motor neurons.
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Loss of VAChT expression is associated with pulmonary inflammation.
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decreased VAChT levels affect synaptic vesicle biogenesis and distribution whereas a lower ACh content affects vesicles shape.
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we conclude that VAChT overexpression is sufficient to enhance ACh release in the hippocampal formation
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Data indicate that elimination of VAChT had only marginal consequences in striatum-related tasks and did not affect spontaneous locomotion, cocaine-induced hyperactivity, or its reward properties.
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Mice with 65% knockdown of VAChT had normal prepulse inhibition and short-term habituation of startle reaction, whereas long-term habituation was disrupted.
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VAChT mutant mice present preserved neuromuscular function, but altered brain cholinergic function and are hyperactive.
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These results reveal the dependence of short-term plasticity on the level of VAChT expression and efficient synaptic vesicle filling.
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Results indicated that VAChT mutant mice have profound cardiac remodeling and reactivation of the fetal gene program.
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Residues 481-490 contain trafficking information necessary for VAChT localization, and within this region L485 and L486 are strictly necessary. Clathrin-mediated endocytosis is required for targeting to microvesicles.
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Real-time RT-PCR revealed significant decreases in VAChT mRNA in the lung of sensitized and allergen challenged animals.
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Vesicular acetylcholine transporter-immunoreactive axon terminals enriched in the pontine nuclei of the mouse.
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Nerve fibers surrounding or within taste buds were immunoreactive for the VAChT antibody.
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results suggest that in rodent prefrontal cortex, the alpha7nAChR plays a major role in modulation of the postsynaptic excitation in spiny dendrites in contact with vesicular acetylcholine transporter containing axons
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VAChT is essential to the normal development of motor neurons and the release of acetylcholine