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eps from blocking the basal ganglia

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i got this off a website off google:

"Neuroleptics (antipsychotics), especially the high potency agents such as haloperidol, induce a variety of involuntary movements known as extrapyramidal side effects. These consist of involuntary movements that occur due to blockade of dopamine receptors in the nigrostriatal pathway of the basal ganglia."

this is getting a bit complicated. apparently the old aps block everything including the basal ganglia. thats where all the eps is coming from. so do the new aps block it less thats why there are fewer eps side effects? or dont they block it at all? plz explain.

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The typical antipsychotics are basically a pretty dirty bomb when it comes to dopamine. They hit everything and they hit it hard. They hit the mesocortex and limbic system. Those areas, when they have too much dopamine, get really excited and hopped up, and that's why you get hallucinations and delusions and things like that. However, dopamine is a great multitasker. It has tons of different roles in different places in the brain. For example, it has a lot to do with movement.

The basal ganglia is a special place in your brain that affects both voluntary (reaching, grabbing, walking) and involuntary (blinking, postural adjustments) movements. Unfortunately, this area also uses dopamine to communicate. This area sends off some dopamine, and that signal means either "hey, get moving!' or "hey, stay still" depending on the specific part of the basal ganglia that's involved and what other parts of the brain it's talking to. Since the APs are so indiscriminate, they'll hit this area hard, and that's why you start to get tremors and twitches and also catalepsy and hypomotor activity.

In terms of specific areas, they have done studies on rats. In the rat, the substantia nigra and the subthalamic nucleus are both silenced by typical antipsychotics, possibly via another area called the globus pallidus. So yes, that citation you found is in the right ballpark.

Typical APs will also elevate your prolactin because in another part of your brain, dopamine is responsible for sending the message "hey, no prolactin please", so if you axe the dopamine, you start to get a lot of prolactin hanging out.

We aren't totally sure yet why the AAPs cause less EPS. One theory is the fast on, fast off theory. Antipsychotics are mostly involved with blocking D2. The typicals hit it hard and stick there for a long time. In fact, the dopamine receptors like typical antipsychotics even more than they like dopamine itself, so if there's haldol around, and dopamine as well, the haldol is going to hang on to those receptors and the dopamine is totally screwed.

The atypicals, on the other hand, bind it with low affinity (they aren't too great at grabbing those receptors and they don't stay on them for too long). In fact, the receptors tend to like dopamine more than they like the AAPs, so if dopamine is around, it still stands a fighting chance. In fact, fighting chance is a good word for it, because the drug and the dopamine have to duke it out. The AAP gets on there, then falls off, and maybe dopamine gets on for a while, then the AAP gets back on. There's a sort of aspect of interplay or compromise between them, unlike the typicals, which just slam in and trash the joint. Which is what you need, sometimes, but it can be hard on the side effects front.

Those receptors DO like the AAPs. If they don't like them enough, you don't get an antipsychotic action. But if they like them too much, you start to get EPS and such. But there's a golden area in the middle, which is where more of the AAPs are. They still help with psychosis, but they allow dopamine to work more normally and still do the things it needs to do to make sure you can think and move properly.

Citation: http://focus.psychia...abstract/2/1/48


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