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Analysis of ML352 inhibitory actions on choline uptake in mouse forebrain synaptosomes yielded similar effects (Vmax 300 nM ML352 = 57.2 ± 3.4%).
In these studies, we found that ML352 inhibited [H]choline uptake with high affinity (Ki = 92 ± 2.8 nM), with data well-fit to a single-site inhibition model (r = 0.935) In Figure 4B, we demonstrate that ML352 choline uptake inhibition was retained when tested in mouse forebrain synaptosomes (Ki = 166 ± 12 nM).
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We thus isolated synaptosome fractions from mouse forebrains and subsequently, synaptosome preparations (SS) were further fractionated into synaptosomal plasmatic membrane (PM), cytosolic (Cyt) and SV fractions.
Open image in new window Figure 2 Reduced cell proliferation and neurogenesis in aged mouse forebrain neurogenic zone.
RNA was extracted from mouse forebrain using Trizol.
Membranes from forebrain synaptosomes and whole brain homogenates also both exhibited a similar NADPH-dependent NO consumption.
However, seeing that the NADPH-dependent responses in cerebellar glia are smaller than in forebrain synaptosomes (see Figures 1C and 1D), regional or cellular differences may exist.
Initial evidence for a modulatory role of RTN1A is provided by our ryanodine binding assays, showing that soluble RTN1523 inhibits the calcium-dependent activation of [H]ryanodine binding in forebrain synaptosomes by 32% (Fig. 7A,B).
We used GeneSpring to identify significantly overrepresented Gene Ontology (GO) categories in the Atrx-null mouse forebrain.
NSCs derived from the dissociation of mouse forebrain samples were suspended in culture medium.
Reduced Cav1.2 expression in the mouse forebrain results in anxiety-like behavior.
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