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Topic: endocytosis

Seminar
2 seminars
ePoster
1 ePoster

In Molecular Neuroscience and Neuroscience

Seminar · Neuroscience

How the presynapse forms and functions”

Volker Haucke · Department of Molecular Pharmacology & Cell Biology, Leibniz Institute, Berlin, Germany

Thu, Aug 28, 2025 · 12:15 UTC

Nervous system function relies on the polarized architecture of neurons, established by directional transport of pre- and postsynaptic cargoes. While delivery of postsynaptic components depends on the secretory pathway, the identity of the membrane compartment(s) that supply presynaptic active zone (AZ) and synaptic vesicle (SV) proteins is largely unknown. I will discuss our recent advances in our understanding of how key components of the presynaptic machinery for neurotransmitter release are transported and assembled focussing on our studies in genome-engineered human induced pluripotent st

Seminar · Neuroimmunology

Microglial efferocytosis: Diving into the Alzheimer's Disease gene pool

Carmen Romero-Molina & Francesca Garretti · Icahn School of Medicine at Mount Sinai

Tue, Dec 20, 2022 · 06:00 UTC

Genome-wide association studies and functional genomics studies have linked specific cell types, genes, and pathways to Alzheimer’s disease (AD) risk. In particular, AD risk alleles primarily affect the abundance or structure, and thus the activity, of genes expressed in macrophages, strongly implicating microglia (the brain-resident macrophages) in the etiology of AD. These genes converge on pathways (endocytosis/phagocytosis, cholesterol metabolism, and immune response) with critical roles in core macrophage functions such as efferocytosis. Here, we review these pathways, highlighting releva

ePoster · Neuroscience

Unifying fast and slow temporal dynamics of AMPARs during Long-Term Potentiation

Surbhit Wagle, Nataliya Kraynyukova, Maximilian Kracht, Anne-Sophie Hafner, Amparo Acker-Palmer, Erin Schuman, Tatjana Tchumatchenko · Bernstein Conference 2024

AMPA receptors (AMPARs) mediate fast excitatory neurotransmission and participate in memory formation. Synaptic strength is proportional to the number of AMPARs in the postsynaptic membrane. Previous models of AMPA receptor trafficking can explain their fast, brief incorporation in dendritic spines after LTP induction but offer limited insights into long-lasting changes in AMPAR content at potentiated spines[1,2]. Hence, a unified modeling framework is necessary to understand persistent synaptic changes in AMPAR numbers. Molecular trafficking, such as diffusion, active transport, endo/exocytos