I just had a wisdom tooth extraction today. My oral surgeon prescribed Tylenol 3, which consists of Acetaminophen and 30 mg Codeine Phosphate for pain control. I just have several questions about the mechanism of action of this medication. From my understanding as a fall 2008 incoming P1 student, codeine itself is an inactive drug, namely a prodrug, that is metabolized in the body into its active form, morphine, by the CYP450 enzyme system. The molecule binds to mu-opioid receptors in the central nervous system to produce analgesic effects. First of all, why exactly is sedation and analgesia produced simply by binding to a mu-opioid receptor? What is the significance of binding to these receptors? Are these receptors somehow connected with GABA and thereby produce sedation by increasing the quantity of this neurotransmitter just like benzodiazepines do? Exactly why am I experiencing the sedation and drowsiness at this very moment? I love the feeling, but I cannot help myself with my curiosity and fascination that comes from just looking at these little white tablets in my orange bottle. Why do slight differences in functional groups on the otherwise similar looking molecule have such a dramatic effect in drug potency? For example, I've read that diacetylmorphine, which is heroin, and contains a similar structure to codeine and morphine, is far more potent than codeine. I obviously knew this, but why does the presence of those two acetyl groups, CH3CO, have any difference in potency? What do those acetyl groups do to make heroin more potent? Sorry about all these questions, but if you guys are truly pharmacy students who love the material, you should be fascinated by all of this and not only view my post, but actually ANSWER IT as well. So, everyone, chime in!