Transcription
So why do you go to sleep? We increase GABA and Gowan in from that VLP. Oh, it's like a sledgehammer. We're turning all the wakefulness apparatus off, and you're going to sleep.
So when you go to sleep, the sedating chemicals should go up. That's what you see here. Your wakefulness chemical, that's the other backup generator, orexin, hypocretin, it lowers. You want the wakefulness chemicals to lower. So throughout the night, this is the kind of thing you want to see. You're like, "Okay, Schwartz, oh, I'm not arousing. I'm asleep."
But why do we go light sleep, deep sleep, light sleep, deep sleep? Why would that happen? This is where it gets fun. Acetylcholine comes in, right? So notice when you're at the bottom of deep sleep and things are being restored, if your brain says, "Hey, we got to get some dreaming in," you get little puffs of acetylcholine. It drives you out of light sleep. That's a stimulating chemical. So the stimulating chemical goes down and puffs up, so you go into dreaming sleep. So you have a pacemaker at night: light sleep, deep sleep.
Look at your other model means dopamine, norepinephrine. Is NR I R those little puffs the driving lights sleep, little puffs? Now they are big puffs. So if I drive up your serotonin, norepinephrine, you get driven into light sleep a lot more. Many of our antidepressants ruin deep sleep, right? Might get eight hours of sleep, your depression lifted, but it's not restorative sleep. You're still tired. Is that a side effect on my drug, or did I ruin your sleep with my therapeutic treatment for depression? So some of the drugs we give can fix this, and some of the drugs we give can hurt this.