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Dopamine Receptors And Their Behavioural Affects

Neuroprotection said:
I think the best approach would be a very slow taper, Maybe even less than 1% reduction each time. very slow tapers over a period of years using liquid drug solutions has been successfully used to get people off SSRI antidepressants which can have severe withdrawals. Also, do you mind describing what the main symptoms you suffer when withdrawing from haloperidol?
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According to https://psychscenehub.com/psychinsights/antipsychotic-withdrawal-syndrome-tapering/

A larger initial dose reduction is doable, but I'll just have to deal with some withdrawals for a while. Then if need be, I can use a liquid formulation to make more hyperbolic reductions after 3-6 months. But I don't actually plan on coming off haloperidol completely. I just want to use a minimum effective dose to reduce side effects and minimise the chance of tardive dyskinesia. And the withdrawals I get are:extreme anxiety, extreme emotions, total insomnia, and some hypertension. That's within the first 72 hours. That is as far as I've gotten. It's possible more symptoms like muscle rigidity will pop up during the first week.
 
I can totally understand your concerns. Obviously you would need to carefully titrate the dose but if it takes a year, it still means you are at a lower risk of developing TD. I shared a house with a guy who was on haloperidol and he most certainly developed TD. I suggested he asked his specialist if an atypical antipsychotic would be a better fit.

Well, it worked BUT. He was a stick thin guy but over the following few years he gained an enormous amount of weight. I would guess olanzapine because in the UK it's the most commonly used neuroleptic in new patients. I think he had been on haloperidol for decades.

So it seems eminently sensible to find the minimum dose of haloperidol that works for you. You have a very positive view of what you want to do and if a 1% reduction works, that's a good idea.
 
Conky said:
According to https://psychscenehub.com/psychinsights/antipsychotic-withdrawal-syndrome-tapering/

A larger initial dose reduction is doable, but I'll just have to deal with some withdrawals for a while. Then if need be, I can use a liquid formulation to make more hyperbolic reductions after 3-6 months. But I don't actually plan on coming off haloperidol completely. I just want to use a minimum effective dose to reduce side effects and minimise the chance of tardive dyskinesia. And the withdrawals I get are:extreme anxiety, extreme emotions, total insomnia, and some hypertension. That's within the first 72 hours. That is as far as I've gotten. It's possible more symptoms like muscle rigidity will pop up during the first week.
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Thanks for that. Just interested to know, do you find being on haloperidol okay or does it kill your emotions? i’ve heard many people say haloperidol strip them of all the joy in their life by causing severe anhedonia. I once read a Study that suggested haloperidol withdrawal in rats made them super sensitive to rewards like sucrose. I know you’ve not got far in antipsychotic withdrawal, but do you know of anyone that has and has this made them more impulsive than they were before.
 
Neuroprotection said:
Thanks for that. Just interested to know, do you find being on haloperidol okay or does it kill your emotions? i’ve heard many people say haloperidol strip them of all the joy in their life by causing severe anhedonia. I once read a Study that suggested haloperidol withdrawal in rats made them super sensitive to rewards like sucrose. I know you’ve not got far in antipsychotic withdrawal, but do you know of anyone that has and has this made them more impulsive than they were before.
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It depends on the dose. 6mg daily is okay. But after I got up to 10mg daily I got severe anhedonia/apathy and I always felt my body was weighed down by something heavy. And of course, every time I tried reducing dose, I would get withdrawals. So I've been using other substances to counter the anhedonia.

And I don't really know anyone else who has gotten haldol withdrawals. There's one person on Bluelight that was on the injection version of haloperidol, but it seems that instead of withdrawal, he continued to feel like he was still on the shot for a long time.
 
The decanoate ester is the depot formulation of haloperidol I believe. Christ alone knows where that ends up. It will redistribute to all the fatty tissue in the body. It's just a crude 70YO medicine. It has it's place in medicine but I'm not sure the depot formulation still has.

As I mentioned before, olanzapine seems to fully substitute. Clozapine is also likely to... but clozapine is best avoided. Suddenly having no white blood cells is a BAD thing.

Oral haloperidol with a tiny taper sounds sensible and practical. Yes it will take a long time but if it improves someone's life then worth it.
 
Conky said:
It depends on the dose. 6mg daily is okay. But after I got up to 10mg daily I got severe anhedonia/apathy and I always felt my body was weighed down by something heavy. And of course, every time I tried reducing dose, I would get withdrawals. So I've been using other substances to counter the anhedonia.

And I don't really know anyone else who has gotten haldol withdrawals. There's one person on Bluelight that was on the injection version of haloperidol, but it seems that instead of withdrawal, he continued to feel like he was still on the shot for a long time.
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Conky said:
It depends on the dose. 6mg daily is okay. But after I got up to 10mg daily I got severe anhedonia/apathy and I always felt my body was weighed down by something heavy. And of course, every time I tried reducing dose, I would get withdrawals. So I've been using other substances to counter the anhedonia.

And I don't really know anyone else who has gotten haldol withdrawals. There's one person on Bluelight that was on the injection version of haloperidol, but it seems that instead of withdrawal, he continued to feel like he was still on the shot for a long time.
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Do you mind me asking what you use to deal with haloperidol induced anhedonia? I ask because I thought strong D2 antagonists diminish the rewarding effects of most recreational drugs.
 
i’ve probably mentioned this 1 million times before, I know I have on other threads but I easily forget, so forgive me. I feel like psychiatric research has focused so much on modulating practically every other brain chemical aside from dopamine. okay, there is some research on dopamine, but that’s mainly for obvious things like ADHD. on the other hand, research is rapidly progressing in the serotonin field and they are looking deeply into downstream effects of serotonin receptors and how to modulate those. same with norepinephrine. I just feel like researchers generally tread much more carefully around dopamine as if there is an unspoken reason as to why potentially hijacking this pathway and subverting tolerance, which is certainly possible is a bad idea. maybe I’m getting into conspiracy here, but I wonder if it’s an ethical thing? for example, serotonin might affect mood stability and empathy whilst norepinephrine mainly deals with components of emotional arousal and cognition. manipulating those neurotransmitters and receptors at will could help us treat many diseases and let us tailor our mood to some extent. on the other hand, I think dopamine is a whole different beast as it’s directly responsible for some of the most powerful components of human desire and drive, with its tentacles reaching into all aspects of emotional regulation, the sleep wake cycle and its influence is equally powerful in both our innate (animalistic desires) and The cognitive parts of our more advanced human brain. imagine if we could manipulate dopamine and its receptors at will. actually, I just got a shiver down my spine whilst writing this but it’s scary in a nice kind of way.
 
like i had chronically low dopamine for a decade and now i take an ad that raises dopa and im no longer a sad sap.

sry im mot very sciency im a dum dim
 
l41n said:
like i had chronically low dopamine for a decade and now i take an ad that raises dopa and im no longer a sad sap.

sry im mot very sciency im a dum dim
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Wow, that’s amazing. You’re a living example of exactly what I was talking about. I just wish psychiatry would take dopamine more seriously in depression treatment. can I ask which medication you take, is it bupropion by any chance?
 
l41n said:
bupropion 150mg each morn and ill consider cycling if tolerance occurs

or 75 if im arcing up
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Yes, I’ve heard so much good things about bupropion, officially, it’s supposed to be as good as the SSRIs although anecdotally people seem to like it much more and benefit from it much more. so long as you take it as directed, hopefully you shouldn’t develop much tolerance to it. if you ever do wish to try something different, or it stops working for you, I would suggest you try selegiline as I’ve heard a lot of good things about that as well. I wish you all the best.
 
Neuroprotection said:
Yes, I’ve heard so much good things about bupropion, officially, it’s supposed to be as good as the SSRIs although anecdotally people seem to like it much more and benefit from it much more. so long as you take it as directed, hopefully you shouldn’t develop much tolerance to it. if you ever do wish to try something different, or it stops working for you, I would suggest you try selegiline as I’ve heard a lot of good things about that as well. I wish you all the best.
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seleg made me manic as fuq 2.5mg orally even once a wk

im bipolar tho, so…

sbf is kinda based ngl
 
Thanks for this interesting thread OP, I have learned a thing or two. My only critique is that, in the future, please write out the full terminology of acronyms before continuing on with just using the acronym. It made it hard to fully interpret what you were saying without having to keep using google.
 
Neuroprotection said:
Do you mind me asking what you use to deal with haloperidol induced anhedonia? I ask because I thought strong D2 antagonists diminish the rewarding effects of most recreational drugs.
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Interesting to note that ketamine is one example of a drug that in animal models, showed self-administration even when the dopamine receptors had been blockaded.
 
Foreigner said:
Thanks for this interesting thread OP, I have learned a thing or two. My only critique is that, in the future, please write out the full terminology of acronyms before continuing on with just using the acronym. It made it hard to fully interpret what you were saying without having to keep using google.
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You’re welcome and thank you for your feedback. Please could you give me an example of where I’ve used an acronym as I’m blind, and my memory is really bad. however, if you point out some examples for me, I can be more careful in future and I will write them out fully.
Thanks again for your feedback.
 
AlsoTapered said:
Interesting to note that ketamine is one example of a drug that in animal models, showed self-administration even when the dopamine receptors had been blockaded.
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Interesting, I’ve not picked up on that before. interestingly, I’ve read that D2 receptors, especially when chronically activated can decrease NMDA currents and reduce the membrane surface of expression of the GLUN2B NMDA receptor subunit. basically, dopamine might actually act like an NMDA receptor antagonist in certain neuron populations in the brain
 
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