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[201] The activated kinases then phosphorylate their respective transporter(s), which in turn causes a conformational change in transporter protein, thereby altering its function and affecting dopaminergic/glutamatergic neurotransmission at dopaminergic synapses

This is considered a favorable alternative to orally bioavailable PDE5 inhibitors that show poor results in subjects with acute metabolic disease [10, 15, 16]

14 When ammonia exceeds the capabilities of the normal hepatic routes for metabolism (primarily the urea cycle), ammonia concentrations increase in the bloodstream and ultimately increase in the brain

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