I’m sure many of you have seen some of my posts on depression pharmacotherapies, the serotonin theory, and the serotonin system. But I’m still getting a lot of questions, and a lot of misconceptions about how the various drugs work. So I’m going to provide a little more information on the types of pharmacotherapies. And this time, you’re also getting PICTURES!
Yup. We’ve been here before.
For further stuff on neurotransmission, take a look at this post. This one isn’t going to cover vesicles or stuff like that. Just get down and dirty with the serotonin.
So as you probably know, neurotransmitters, like serotonin, are released into the synapse. Like this:
Now here is where people get mixed up. A neurotransmitter, in itself, is just a chemical. It doesn’t MEAN anything on its own. It’s just a chemical, and could be anything, really. No, what’s important about transmitter is the effects it has on a receptor.. So it doesn’t matter how much or how little transmitter you have anywhere, if there is no receptor to interact with it. Like this:
Now, that neurotransmitter can’t hang around forever, it needs to be broken down or taken away, or it will keep stimulating the receptors. You don’t want that, normally, you want a reaction to be short and sweet and done. So you have transporters:
Those little blue things. Those suck up the serotonin back into the presynaptic neuron to be used again, or broken down.
So now let’s talk about SSRIs, Selective Serotonin Reuptake Inhibitors. These drugs, including things like Prozac, Celexa, Lexapro, Zoloft, and Paxil, just to name some big ones, all have their primary mode of action by BLOCKING the serotonin transporter. When I said this before, I had some people thinking that this would LOWER the levels of serotonin in the synapse. Quite the reverse:
The serotonin transporter can’t bring up serotonin anymore. This means that, as more serotonin is released through natural cell firing, serotonin is going to build UP in the synapse:
And with all that serotonin around, the receptors on the postsynaptic neuron are going to be stimulated a lot more than they would be normally. So this means that they effects of serotonin become a lot BIGGER than they might be otherwise. And this can help some of the symptoms associated with depression. We used to think that this was because depression was caused by low levels of serotonin. But we now think that, if there ARE low levels of serotonin associated with depression, these might be part of the symptoms rather than the source of the problem. Thus, treating some of the neurochemical symtoms can still help the symptoms that a person with depression might experience, but they don’t necessarily SOLVE the problem of depression. For that, we’re still doing research.
