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How potent is Bupropion/Welbutrin?

For 300, I've just been taking two in the morning.

So, two SR at the same time.
I certainly don''t intend to split the dose and take one before bed.
 
paranoid android said:
About the only time you will notice a difference in different brands of Bupropion in terms of efficiency and potency is if you say switch to a Extended 24 hour release version of it if you have previously been on the 12 hour Sustained release version or vice versa. Some people do find that the XR version of Bupropion (Wellbutrin XR and various generics) is not as strong as the SR version or as effective in treating Depression. I found this to be somewhat true as the SR version is abit rougher for lack of a better word and has more stimulation which is not a bad thing if you are suffering from Bipolar Depression or SAD.
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I''ve been scouring for any kind of clinical data on this but, literally cannot find a single relevant piece of clinical information apart from the (very) occasional anecdotal report.

Not questioning your opinion.
I just want something concrete to present to my consultant.
 
Ho-Chi-Minh said:
WB is for all intents and purposes an NRI until it reaches 450+mg, and even then it doesn't bind with much efficacy to DAT
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Alrighty.....

Having recently titrated to 450mg - and been KTFO, this piece of information intrigues me greatly.

And I would have to chase it up by asking - where did you attain it?
Clinical trial data?
Pharmacology book?
And do you have a link for that source?

At 450 - it was sedating.
Before that, it was activating.

That would of course suggest that dopamine does not incite an activating response in myself - much like serotonin.
The opposite, in fact.

That being said, it's a reuptake inhibitor at that dose right?
What - doesn't that mean a decrease in the release from the presynaptic neuron, but a greater concentration ultimately manifesting itself in the synaptic cleft?

I'm trying to discern how that differs from a dopamine agonist - in pramipexole - which also had the effect of knocking me for six.
Agonist meaning, increase the activity of the dopamine receptor above basal level....
Which produces more of it??
 
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Agonists have different affinity for different dopamine receptors and different efficacy for activating the different pathways that the dopamine receptors can signal through when bound by an agonist.

A reuptake inhibitor is going to have differential effects because the locale of the effect is dependent on dopamine transporter expression, for example there is minimal dopamine transporter expression in the PFC, dopamine reuptake there is handled by the norepinephrine transporter, so am NRI somewhat selectively increases dopamine in the PFC (as far as purely reuptake inhibiton related effects, ignoring downstream effects of increasing NE). Although norepinephrine can bind to dopamine receptors as well, though this could be less than 5% as potent as dopamine.

I can't recall the affinities but I do recall nicotinic acetylcholine receptor antagonism was suspected to play a role in WB's effects as well.
 
I recall also, when I titrated up to 300mg of venlafaxine - the dose at which dopamine comes into play, supposedly, that also had a highly sedating effect on me.
Having seen this being reflected in pramipexole use, and now 450 mg bupropion use - could that potentially solidify an opinion that, in terms of my personal reaction to dopamine - it's ultimately sedating?

I was on the fence about serotonin in that capacity for a while also but, after so many serotonergics yielded the same fatigue inducing effect - I'm pretty much forced to draw that conclusion...
 
From wiki mirtazipine page:

5-HT2C inverse agonists have been shown to inhibit mesoaccumbens dopamine outflow[101]

Does that mean remeron inhibits dopamine?
If so, possibly a reason I responded favorably to it...?
Given my unfavorable response to dopamine activators...?
 
I thought in general the 5-HT2C receptors inhibited dopaminergic neurons, if I recall correctly VTA dopaminergic neurons have 5HT2C receptors on them that inhibit the cell when activated. These 5-HT2C receptors in the medial prefrontal cortex could be functioning fairly opposite to what is usually thought about 2C. I thought 2C receptors in the VTA itself were supposed to inhibit dopamine and NE in the VTA.

The theory behind 5HT2A / 5HT2C over expression sometimes observed in depressed people (suicide victims) I think has partly to do with both of said receptors being able to inhibit neurotransmitters in some cases, but I'm sure there are exceptions to every rule.

The last thing I should mention is that I don't know whether mirtazapine is an antagonist or an inverse agonist. I know that most antagonists are really inverse agonists when it comes to 5-HT2A but I don't know if 5-HT2C receptors are atypical as well.
 
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farmacista said:
there's also reboxetine as a noaradrenergic that should be available in europe
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I'm
I'm actually gonna bump this thread on the basis of this response.

In Stahls Essential pharmacology - he seems to think that a combination of reboxetine and wellbutrin, would potentiate the effect of noradrenaline RI, or release - or whatever mechanism they incorporate.
But he seemed to this potentiation would be a product of their combination.

Does anyone have experience with Reboxetine?

It carries a very low side effect profile, so would appeal in that sense.

Mixed reports regarding efficacy - in particular one meta-analysis trial, which yielded results of reboxetine being 2x as less effective than its AD counterparts.
It did not delineate the efficacy of wellbutrin as a comparator, however.
 
Psychiatry is far from an advanced science. I don't remember that post or my source. But I know that the catcholamines are similar enough that generally speaking, increasing dopamine will lead to an increase in norepinephrine, and norepinephrine, an increase in dopamine. I don't know about the summation of this activity in relation to blocking some of the nicotine sites.

It's a funky compound.

Leave it to your doctor. None of us figure things out through a biochemical level.
 
Ho-Chi-Minh said:
Psychiatry is far from an advanced science. I don't remember that post or my source. But I know that the catcholamines are similar enough that generally speaking, increasing dopamine will lead to an increase in norepinephrine, and norepinephrine, an increase in dopamine. I don't know about the summation of this activity in relation to blocking some of the nicotine sites.

It's a funky compound.

Leave it to your doctor. None of us figure things out through a biochemical level.
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I'm
I'm beginning to see this.

Reviewing those neuroscience/pharmacology books - shit is fucking cake compared to engineering (my major).
 
I'll say that it's so unlike "real" stimulants that it's not officially indicated to treat stimulant addiction.
 
I have been taking Wellbutrin for about 7 months. It was extremely effective in dealing with my anhedonia, hipolibidemia, and apathy. But all of a sudden it stopped working :-( I guess I've become tolerant to it, due to receptors downregulation.Suppose that I want to stop the tolerance growth and upregulate dopamine receptors, without quitting Wellbutrin (I had one attempt - side effects were awful)
-Is It possible at all or do I need 'drug vacation' from Bupro (for how long if necessary)?? :-/
-How should such a "repair" program look alike? (supplementation, droses, taking regimen)

Currently my tolerance build up prevention follows: 250 mg of magnesium taurate and 800 mcg of Forskolin before bedtime. Results are miserable. Therefore I added 60 mg of zinc, but also the effects are poor.
I tried turmeric and cinnamon in mega doses - my digestive system couldnt bear it.

I dont have access to DXM or memantine, also would fear side effects, like f.e. respiratory depression.
What should I do next? Need advice, help :-(
 
DXM?

Can you even take that with bupropion?

In fact, can you take it with a mirtazapin/bupropion combo?
 
There is the risk of serotonin syndrome and then lowering the seizure threshold (from NRI). Depending on the Mirtazapine dose the serotonin risk would be minimal in my opinion (if it was say 30mg).

The dose of DXM would be important, and I wold be important to start out low (25mg, then trying a bit more another day etc.) Other opinions are more than welcome here, but I would personally think that you could take less than 100mg DXM on a 300mg bupropion 45mg mirtazapine combo. The mental health/hypomania stuff is probably the concern.
 
DXM: Some users report it lowers or reverse tolerance to adderal and other drugs affecting dopamine&norepinephrine, so it might work well with buproprion an NDRI.
Memantine (nootropic) has the same effect, but both are expensive and really hard to get, so I am looking for easier solution.
I find Wellbutrin a life changing drug for someone dealling with longterm permanent depression, but it has 1 drawback: it is shortterm, you become tolerant within couple of years (if You have luck), in my case it was 4 months.
 
lamia666 said:
DXM: Some users report it lowers or reverse tolerance to adderal and other drugs affecting dopamine&norepinephrine, so it might work well with buproprion an NDRI.
Memantine (nootropic) has the same effect, but both are expensive and really hard to get, so I am looking for easier solution.
I find Wellbutrin a life changing drug for someone dealling with longterm permanent depression, but it has 1 drawback: it is shortterm, you become tolerant within couple of years (if You have luck), in my case it was 4 months.
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Is
Is that for real?
Can anyone else back that up?
 
That's kinda what I was getting at earlier about long term antidepressant efficacy versus achieving reduction of a score on a depression inventory at 1 month :( I'm under the impression that dopaminergics generally don't have too much long term efficacy, though you might get a couple years out of them. SSRIs/SNRIs on the other hand result in genetic changes that can give rise to long term efficacy, where you can taper off and be in unmedicated remission.
 
Ho-Chi-Minh said:
But I know that the catcholamines are similar enough that generally speaking, increasing dopamine will lead to an increase in norepinephrine, and norepinephrine, an increase in dopaminel
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Norepinephrine is even an agonist at dopamine receptors, although with wide differences between dopamine receptors (there are quite a few dopamine receptors, and then there are the amphetamine induced/schizophrenia associated dopamine receptor high affinity states).
 
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