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To achieve this, we first compute surface normals to all triangles on the surface of the neuron.
We hypothesize the fluctuations of UNC-40 activity cause fluctuating sites of axon outgrowth and thus a succession of imbalanced outwards force across the surface of the neuron.
Images were collected at the rate of one image/min from a single optical section (<3 μm) near the surface of the neuron.
Proteins called AMPARs, which are found on the surface of the neuron, can detect glutamate and transmit the signal along the second neuron.
In theory, random fluctuations of the site of axon outgrowth over time create a fluctuating force at the surface of the neuron, allowing positional changes to be modeled as a random walk (Box 1).
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The pathogenesis of Alzheimer's disease is closely associated with the accumulation of amyloid-β (Aβ) peptides, which eventually form neuronal deposits known as senile plaques on the outside surface of the neurons [1] and lead to neuron death.
Such approaches targeted only the surface of the neurons.
When Galic et al. engineered rat neurons to produce more of the ArhGAP44 protein, fewer filopodia formed on the surface of the neurons.
The chemicals diffuse quickly across the minute gap between the neurons and dock with receptors on the surface of the receiving neuron.
This resting potential contribution is proportional to the total surface area of the neuron.
These neurotransmitters bind to receptor proteins on the surface of the second neuron and control how it fires.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com