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This experiment alone does not eliminate the possibility NO affects cells presynaptic to B31/B32, or that Ca+2 dependent spikes which are not blocked by TTX are releasing NO at rest from neurons presynaptic to B31/B32.
Such experiments showed that these neurons produce NO at rest, and NO contributes to their resting potential.
These experiments strongly suggest that B31/B32 neurons are themselves nitrergic, and produce NO at rest, in the absence of firing and Ca+2 entry into the cell.
Why actively inhibit feeding-related neural activity via the constant production of NO at rest, in the absence of stimuli that elicit the behavior?
Since no other neuron was present, this experiment demonstrates that C-PR also contains an isoform of NOS that is active and produces NO at rest, in the absence of firing.
However, treatment with NO blockers did excite cerebral ganglion neuron C-PR, a command-like neuron initiating food-finding behavior, both in situ, and when the neuron was cultured in isolation, indicating that this neuron also inhibits itself by producing NO at rest.
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The muse was no longer at rest, but had possibly departed.
We demonstrated that Δ594 604 and Δ605 612 constructs in non-stimulated cells displayed higher levels of NO2−/NO3− accumulation when compared with WTeNOS and other constructs, indicating that Δ594 604 and Δ605 612 could produce NO at a resting state of calcium concentration.
The patient continued on oral co-trimoxazole alone until a total of 12 months of treatment had been completed, at which stage she had no pain at rest and there were no sinuses or discharge from the foot, although there was still considerable residual bony abnormality evident radiologically.
Applying an NO scavenger to quiescent Aplysia buccal ganglia initiated fictive feeding, indicating that NO production at rest inhibits feeding.
In patients who have no symptoms at rest and only mild symptoms while exercising (sometimes called incipient heart failure), salt restriction and diuretics may be sufficient.
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