Publications by authors named "M Verhage"

Sorting nexin 4 (SNX4) is an evolutionary conserved organizer of membrane recycling. In neurons, SNX4 accumulates in synapses, but how SNX4 affects synapse function remains unknown. We generated a conditional SNX4 knock-out mouse model and report that SNX4 cKO synapses show enhanced neurotransmission during train stimulation, while the first evoked EPSC was normal.

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Mutations in the microtubule-binding motor protein kinesin 5 A (KIF5A) are implicated in several adult-onset motor neuron diseases, including Amyotrophic Lateral Sclerosis, Spastic Paraplegia Type 10 and Charcot-Marie-Tooth Disease Type 2. While KIF5 family members transport a variety of cargos along axons, the specific cargos affected by KIF5A mutations remain poorly understood. Here, we generated KIF5Anull mutant human motor neurons and analyzed the impact on axonal transport and motor neuron outgrowth and regeneration in vitro.

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Negative birth experiences are common. It is yet unclear which women may be most at risk already before pregnancy. Childhood trauma and non-autonoumous/unresolved attachment state of mind may affect how women experience giving birth.

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Article Synopsis
  • Neuropeptides and neurotrophins are released from dense core vesicles (DCVs), and recent research highlights the unique role of the RAB3-RIM1 pathway in DCV exocytosis, differentiating it from the synaptic vesicle (SV) exocytosis mechanism.
  • The study identifies rabphilin-3A (RPH3A) as a negative regulator of DCV exocytosis, where its absence led to a threefold increase in DCV release in RPH3A deficient neurons.
  • RPH3A's role in regulating DCV exocytosis is linked to its interaction with SNAP25; although it is not needed for DCV transport, its binding to SNAP25 is
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Mutations in the microtubule binding motor protein, kinesin family member 5A (KIF5A), cause the fatal motor neuron disease, Amyotrophic Lateral Sclerosis. While KIF5 family members transport a variety of cargos along axons, it is still unclear which cargos are affected by mutations. We generated null mutant human motor neurons to investigate the impact of KIF5A loss on the transport of various cargoes and its effect on motor neuron function at two different timepoints .

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