The drug, labeled CX717 (Cortex Pharmaceuticals), acts on AMPA receptors, protein structures on the surface of neurons. When these receptors bind to the neurotransmitter glutamate, they transduce excitatory signals by opening an ion channel. Ampakines including CX717 make the activated channel stay open longer when glutamate binds. More ions pass through the channel, creating a stronger signal when nerve cells are activated. The ubiquity of these receptors makes them good targets for drugs that increase general cognitive functioning.
The researchers used a technique called positron emission tomography, or PET, to gain insight into CX717's neurobiological role. The PET signal reflected the distribution and rate of metabolism of ingested radioactively labeled glucose in the monkeys' brain cells. By measuring regional brain glucose metabolism, the researchers determined that for sleep-deprived monkeys, glucose metabolism drops off in brain areas previously associated with memory tasks—namely, the prefrontal cortex, the dorsal striatum, and the medial temporal lobe. However, when sleep-deprived monkeys took the drug, they showed heightened glucose metabolism in these same brain regions. The researchers compared these results to suggest a biological basis for the drug's effects.
Previous studies have shown that caffeine and amphetamine can reduce the deleterious cognitive effects of sleep deprivation. But as anybody who has indulged one latte too many knows, caffeine and other powerful stimulants have limited usefulness. These potentially addictive chemicals can distort thinking just as they can enhance it. Because CX717 has a different biochemical action, it may be more beneficial than stimulants