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This image reconstruction approach leads to the conclusion that the cerebellar spine necks are unlikely to reduce transfer of synaptic charge by more than 5-205-20%en if their smooth endoplasmic reticulum were to completely block passage of current through the portion of the neck that it occupies.
Furthermore, STP and LTP have different functional consequences for the transfer of synaptic information in that STP modulates the frequency response (Volianskis et al., 2013b) whereas LTP provides amplification whilst preserving the fidelity of synaptic transmission (Pananceau et al., 1998; Selig et al., 1999; Volianskis et al., 2013b).
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RRP size was determined by measuring the charge transfer of the transient synaptic current induced by a pulsed 5 s application of hypertonic solution (500 mM sucrose in extracellular solution).
Additionally, the slight transfer of changes in synaptic strength from one stimulus position to the next within a receptive field can be explained by partial overlap of the inputs activated by different stimuli as previously suggested (Meliza and Dan, 2006).
Briefly, to obtain the fraction of RRP released at 250 mM sucrose solution, the charge transfer of the transient synaptic current was measured and divided by the RRP size obtained by 500 mM sucrose application (5 s) from the same neuron.
It emerges that L2-R feedback over the first 20 s of naturalistic stimulation was necessary for sensitivity control of synaptic signal transfer, boosting the R1 R6 and LMC outputs by ∼15% and ∼40%, respectively.
Adding yet other orthogonal markers, such a calcium indicators, should make it possible to see the ontogeny of synaptic information transfer across the specific cells in the developing circuitry of the retina.
These observations suggest that the presence of amyloid pathology enhances the trans-synaptic transfer of tau in vivo.
The hierarchical pathways of NFD in tauopathies might be associated with the trans-synaptic transfer of Tau pathology, as recently suggested in vivo[ 20, 21].
Such differential behaviour between the two Tau species also supports the in vivo specific trans-synaptic transfer of soluble Tau species rather than aggregates, as suggested using WT V5-Tau.
In conclusion, independent of the mechanisms involved in Tau spreading, we demonstrated for the first time in vivo that the specific trans-synaptic transfer of Tau protein from degenerating neurons might lead to the preliminary steps of Tau pathology in secondary neurons.
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