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We therefore wondered if ambient glutamate could activate a tonic NMDAR-mediated current in cortical neurons and whether or not this current is mediated selectively by GluN2B-containing NMDARs?
The Ca2+ current is mediated by CatSpers while the K+ current is mediated presumably by mSlo3.
This latter result excludes the possibility that the current is mediated by endogenous TRPM8 in non-transfected neurons, and no published evidence currently indicates endogenous TRPM8 expression in rodent hippocampus.
Moreover, the NMDA and glutamate excitotoxicity is absent in retinal ganglion cells, which lack syn-NMDAR, and the NMDAR current is mediated by receptors at the extrasynaptic sites.
We assessed anion selectivity experiments to determine whether the voltage- and Ca2+-dependent macroscopic current is mediated by a chloride channel.
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For the biofilms grown under 0.2 V, differential pulse voltammetry showed that the metabolic current was mediated by interfacial cofactors with mid-point potential around −0.16 V performing single-electron electron transfer (ET).
Additional evidence that these current was mediated exclusively by KAR was provided by the fact that the remaining current was unaltered during application of the AMPAR desensitization blocker CTZ.
These results suggested that the dexmedetomidine-induced outward current was mediated by α2-adrenoceptors.
These findings suggested that the dexmedetomidine-induced outward current was mediated by K+ channels through the activation of G-proteins.
To test the idea that a component of the outward current was mediated by KCNQ channels, XE991 (3, 10 and 30 μM) was applied to the cell.
Superfusing yohimbine (4 μ m) alone accelerated the recovery of outward currents to baseline level (Fig. 2Cand D), confirming that the dexmedetomidine-induced current was mediated by α2-adrenoceptors.
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CEO of Professional Science Editing for Scientists @ prosciediting.com