To answer this question, we need to have general knowledge of how biochemical receptors function in the body, specifically melatonin receptors, as well as some feedback mechanisms the body uses when homeostasis is disrupted.
A. The passage states that these two drugs combat insomnia by activating melatonin receptors. If we didn’t already know this, melatonin receptors signal the brain to tell us we are sleepy. This is kind of similar to if we took melatonin itself, but since these people suffer from insomnia, they probably need something that binds to these receptors more strongly. These drugs are melatonin receptor agonists. To answer the second part about side effects, we can see that the passage does not tell us what the side effects are (and since these are fictional drugs, we can’t look that up). Based on my preliminary research in the source below, there is not yet a definitive answer to how exactly MT1 and MT2 activation differ in their overall effects on the body. So, the question is likely just asking us to say that most of the side effects are mediated through MT2 activation instead of MT1, since Byphodine (which has more side effects) activates MT2 more frequently due to its affinity.
B. The body is constantly monitoring its number of receptors through complex processes. Since it can sense that more than the usual physiological amount of MT1 receptors are bound and activated, it “thinks” that it needs more receptors to function normally. Potentially, this would mean that signaling becomes dampened. Meaning, if normally the effect of becoming “sleepy” only needed 50 activated MT1 receptors, after four days it may need 100 to reach the same “sleepy” effect. The second part is talking about the signaling cells, or the cells that normally are releasing melatonin. What could happen is that the body senses that since MT1 receptors are being activated, that we “have enough” melatonin, as the downstream “sleepy” cellular mechanisms are saying so. What could happen is that they stop producing melatonin naturally. We see this in a lot of drugs that we take—for instance steroids. When we take exogenous steroids, signaling in our body tells us that we “have enough” steroids, so we don’t need to produce any more. This is an example of a negative feedback mechanism.
Fun fact: Byphodine and Dehalcynate are fictional drug names used in TV and movies before!
Sources:
Liu, Jiabei et al. “MT1 and MT2 Melatonin Receptors: A Therapeutic Perspective.” Annual review of pharmacology and toxicology vol. 56 (2016): 361-83. doi:10.1146/annurev-pharmtox-010814-124742
