The leading example of modafinil is erroneous. Modafinil works by at least 3 mechanisms. Part of the complexity is because we don’t yet fully understand how an

The leading example of modafinil is erroneous. Modafinil works by at least 3 mechanisms. Part of the complexity is because we don’t yet fully understand how and what causes sleep; or why it is so necessary that without it you will surely die. So balancing what does what it (modafinil) works by is difficult, however possibly the greatest contribution to our understanding of the mechanism governing the drive towards sleep has been modafinils insights into this: As you go about your day, adenosine (yes, the dna base) accumulates in the extracellular space in the brain. These levels reach a peak before you sleep; sleeping allows re-uptake/cleaning of intracellular adenosine. Theories have proposed that levels of intracellular adenosine contribute to the drive to sleep/fatigue. Caffeine binds as an antagonist to the adenosine receptor; which is where the stimulant effect is derived from. Modafinil causes re-uptake of adenosine; so there is less intracellular adenosine bonding adenosine receptors (and presumably causing the reverse of stimulation), a function normally carried out at night. There are at least two other known functions since I last did an enormous deep dive in modafinil and read every published paper during Med school