SZ is hypothesized as having too much dopamine in our brain. So, we are prescribed medicine to essentially block the dopamine, which in turn, produces even MORE dopamine. THIS, causes our brains to have very low amounts of the chemical.
It’s a bit more complicated. There’s agonists and antagonists. So some things jump on the receptor and occupy them thus relieving symptoms but then there’s Parkinsons which is kinda the opposite and too few dopamine. Some people on meds get the parkinsons symptoms from the meds…so it’s not just simply blocking or unblocking dopamine…
There’s also chemicals which are partial antagonists/agonists…I get confused on which is what but they confuse the receptor to being occupied when it isn’t really.
I’m sure someone else will have a more scientific explanation but I wonder these days that increasing dopamine behavior increases symptoms…? I’m not sure there’s an easy answer to that one.
That acts on the D1 receptor, but there is no mention of APs acting on that receptor anywhere.
I guess you’re right, there could be partial agonists etc etc.
Damn, it feels like I’m in college again trying to understand this shiit. I probably never will, but it’s nice to get a little bit more than the generalized idea of it.
From what I’ve read D2 and D4 are the major ones the meds work on. It was found before the meds or maybe with them that dopamine was prevalent in schizophrenic brains. It’s an interesting thing the history of meds. Thorazine was rather brutal but with haldol it was a bit better for function. I still have seen others into the last 10 years still on haldol.
Why things work for some and not others is probably the more pertinent question. You win that one and you’ve a Nobel prize for sure…
Dopamine is not a feel-good neurotransmitter. That’s probably the most common misconception when it comes to neurotransmitters. Dopamine mainly regulates motivation and learning. Feeling good comes more from endorphins and serotonin receptors innervating dopamine circuits.
@anon57786250 IIRC, antipsychotics work on D2 by decreasing dopamine D2 transmission, but increases in D3 or D4 dopamine transmission (not sure which or both) are also associated with therapeutic effects in APs. Also, some APs’ antipsychotic effects work mainly through serotonin receptors, because serotonin circuits are major modulators of dopamine transmission.
Also, remember that sz is associated with lowered levels of dopamine in some areas, that receptors have subgroups that can work in very different ways, and that although it is interesting to read about AP receptor affinities, the long-term therapeutic effects of most psychiatric meds including APs are more likely due to changes in genetic expression than their direct effects on receptors.
Ahh okay, thank you! Are these people doing these fasts actually accomplishing anything then? To me they just seem really pointless but I’m no expert, haha. I guess I say that out of jealousy because my dopamine production isn’t normal.