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Wellbutrin + Abilify combo

trainman04

Bluelighter
Joined
Dec 18, 2017
Messages
189
Would this be a good Combo Mainly for depression.
I was thinking 300mg wellbutrin with low dose abilify 10mg.
Im looking to increase my dopamine production.
 
Abilify is an antipsychotic. It will block several dopamine receptors, and only partially activate others.

Wellbutrin actually only has very weak effects on dopamine. Oh, it might bind to dopamine transporters in-vitro, but in-vivo (in the human body), it is rapidly converted to hydroxybupropion, which is still an effective noradrenaline reuptake inhibitor but almost devoid of dopaminergic activity.
 
Abilify is an antipsychotic. It will block several dopamine receptors, and only partially activate others.

Wellbutrin actually only has very weak effects on dopamine. Oh, it might bind to dopamine transporters in-vitro, but in-vivo (in the human body), it is rapidly converted to hydroxybupropion, which is still an effective noradrenaline reuptake inhibitor but almost devoid of dopaminergic activity.
where does it say block several dopamine receptors? its a partial agonist .

Wouldnt Ablify be a good way to increase Dopamine if your dopamine is low? In combination with wellbutrin. I thought it helped with balance more so increase dopamine than decrease it.,
 
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where does it say block several dopamine receptors? its a partial agonist .

Wouldnt Ablify be a good way to increase Dopamine if your dopamine is low? In combination with wellbutrin. I thought it helped with balance more so increase dopamine than decrease it.,

I looked it up again: As far as serotonin receptors are concerned, Abilify is a partial agonist at 5HT1A and an antagonist at 5HT2A, 5HT2B and 5HT7. With dopamine it will selectively bind to D2, however there is evidence that rather than "partial agonism", its action might be best described as "functional selectivity" - it will act as an agonist where dopamine is too low, and an antagonist where dopamine is too high.

It's not really a "dopamine booster" except at neurons where dopamine is very low, as far as I know. There are cases where abilify has induced parkinsonism, so that would suggest that generally there is more blocking than activating going on on average.

It is certainly a drug worth trying, and it may very well help with your anxiety, just probably not in the way you think (i.e. it won't boost your dopamine to the point where it counteracts your serotonin, especially since it is also a partial agonist at the 5HT1A serotonin receptor).
 
I looked it up again: As far as serotonin receptors are concerned, Abilify is a partial agonist at 5HT1A and an antagonist at 5HT2A, 5HT2B and 5HT7. With dopamine it will selectively bind to D2, however there is evidence that rather than "partial agonism", its action might be best described as "functional selectivity" - it will act as an agonist where dopamine is too low, and an antagonist where dopamine is too high.

It's not really a "dopamine booster" except at neurons where dopamine is very low, as far as I know. There are cases where abilify has induced parkinsonism, so that would suggest that generally there is more blocking than activating going on on average.

It is certainly a drug worth trying, and it may very well help with your anxiety, just probably not in the way you think (i.e. it won't boost your dopamine to the point where it counteracts your serotonin, especially since it is also a partial agonist at the 5HT1A serotonin receptor).
but doesent partial agonist at the 5HT1A receptor decrease serotonin doesent it activate the autoreceptors ?
I heard abilify was weak on serotonin... I heard low dose is better for increasing dopamine and higher dose block more...
 
Generally, drugs that are developed with 5HT1A partial agonism are partial agonists at post-synaptic heteroreceptors and antagonists at pre-synaptic autoreceptors. Antagonizing pre-synaptic 5HT1A receptors causes more serotonin release which is compounded by the post-synaptic partial agonism.

Additionally, aripiprazole as you indicated is a partial agonist at dopamine receptors, meaning as you said its effects are antagonistic when dopamine levels are high and agonistic when dopamine levels are low. However, the intrinsic activity (measured as a percent) can help us to determine if a compound has more activating potential or more blocking potential. Aripiprazole has an intrinsic activity at D2 around 60% which makes it more of an activator. However, it's "cousin" brexpiprazole has intrinsic activity at D2 closer to 40% making it more of a blocker. This is one of the reasons why those who experience agitation or over-activation from aripiprazole but do improve otherwise may actually be better off switching to brexpiprazole. Tolerability was generally better. It does have more weight gain than aripiprazole but less incidence of akathisia.

Another good thing to note is that aripiprazole increase COMT gene expression. COMT is responsible for breaking down dopamine so aripiprazole doesn't necessarily translate into higher dopamine
 
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