Synaptotagmin-1 is a Ca2+ sensor for somatodendritic dopamine release

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A cell-type-specific alternative splicing regulator shapes synapse properties in a trans-synaptic manner

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Astrocytes mediate cell non-autonomous correction of aberrant firing in human FXS neurons

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Mutations in the transcriptional regulator MeCP2 severely impact key cellular and molecular signatures of human astrocytes during maturation

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Unc13A dynamically stabilizes vesicle priming at synaptic release sites for short-term facilitation and homeostatic potentiation

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DRD1 signaling modulates TrkB turnover and BDNF sensitivity in direct pathway striatal medium spiny neurons

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Differential roles of CaMKII isoforms in phase separation with NMDA receptors and in synaptic plasticity

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Organelle mapping in dendrites of human iPSC-derived neurons reveals dynamic functional dendritic Golgi structures

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Activity-dependent release of phosphorylated human tau from Drosophila neurons in primary culture

Neuronal activity can enhance tau release and thus accelerate tauopathies. This activity-dependent tau release can be used to study the progression of tau pathology in Alzheimer''s disease (AD), as hyperphosphorylated tau is implicated in AD pathogenesis and related tauopathies. However, our understanding of the mechanisms that regulate activity-dependent tau release from neurons and the role that tau phosphorylation plays in modulating activity-dependent tau release is still rudimentary. In this study, Drosophila neurons in primary culture expressing human tau (hTau) were used to study activity-dependent tau release. We found that hTau release was markedly increased by 50 mM KCl treatment for 1 h. A similar level of release was observed using optogenetic techniques, where genetically targeted neurons were stimulated for 30 min using blue light (470 nm). Our results showed that activity-dependent release of phosphoresistant hTau^S11A was reduced when compared with wildtype hTau. In contrast, release of phosphomimetic hTau^E14 was increased upon activation. We found that released hTau was phosphorylated in its proline-rich and C-terminal domains using phosphorylation site-specific tau antibodies (e.g., AT8). Fold changes in detectable levels of total or phosphorylated hTau in cell lysates or following immunopurification from conditioned media were consistent with preferential release of phosphorylated hTau after light stimulation. This study establishes an excellent model to investigate the mechanism of activity-dependent hTau release and to better understand the role of phosphorylated tau release in the pathogenesis of AD since it relates to alterations in the early stage of neurodegeneration associated with increased neuronal activity.     

A synaptic molecular dependency network in knockdown of autism- and schizophrenia-associated genes revealed by multiplexed imaging

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Efficient generation of lower induced motor neurons by coupling Ngn2 expression with developmental cues

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Astrocytic cell adhesion genes linked to schizophrenia correlate with synaptic programs in neurons

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Axonal mRNA binding of hnRNP A/B is crucial for axon targeting and maturation of olfactory sensory neurons

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NOVA1 acts on Impact to regulate hypothalamic function and translation in inhibitory neurons

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Longitudinal development of the cerebellum in human infants during the first 800 days

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Time-dependent and selective microglia-mediated removal of spinal synapses in neuropathic pain

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SARS-CoV-2 Spike protein induces TLR4-mediated long-term cognitive dysfunction recapitulating post-COVID-19 syndrome in mice

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Innate and learned odor-guided behaviors utilize distinct molecular signaling pathways in a shared dopaminergic circuit

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