Why does bupropion/wellbutrin also cause PSSD, and therefore why don't dopamine agonists?

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gaydolphinorgy
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Why does bupropion/wellbutrin also cause PSSD, and therefore why don't dopamine agonists?

Unread post by gaydolphinorgy »

We know that SSRIs cause it but bupropion/wellbutrin acts on dopamine/norepinephrine, not serotonin, unlike SSRIs.

And if bupropion can cause it, then why do dopamine agonists like pramipexole not cause it?

Something is missing here.

Edit:

I found an interesting comment on drugs.com

"David
August 11, 2018
“46 year old male. Started taking Bupropion (branded as Zyban) to help stop smoking. Unfortunately, within 1 day I completely lost the ability to o orgasm. I persisted once and 'forced' an orgasm. I immediately had an awful migraine-like headache. I suspect that those who find Bupropion helps their sex life, had low dopamine levels; Bupropion increases the effects of dopamine. For those like me, where Bupropion has killed their sex life, I suspect dopamine levels were already high - If you take a NDRI when you already have high dopamine levels, it will kill your libido/ability to orgasm, as the brain literally thinks you are always 'post-orgasm'! Orgasm is the point when the brain releases the most dopamine (narcotic drugs aside). If dopamine levels are too high, the brain thinks you have recently reached orgasm and will not allow you to orgasm (easily) to prevent very high dopamine levels, which can be harmful (can cause psychosis). This drug is certainly not for me.”
Gameclay
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Re: Why does bupropion/wellbutrin also cause PSSD, and therefore why don't dopamine agonists?

Unread post by Gameclay »

AFAIK there's a study which shows bupropion desensitizes 5ht autoreceptor. Personally I took it for 2 months and didn't feel anything though
BlackCat
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Re: Why does bupropion/wellbutrin also cause PSSD, and therefore why don't dopamine agonists?

Unread post by BlackCat »

Don't they recommend Welbutrin as an antidepressant that WON'T f*ck up your libido?
Area1255_2021
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Re: Why does bupropion/wellbutrin also cause PSSD, and therefore why don't dopamine agonists?

Unread post by Area1255_2021 »

gaydolphinorgy wrote: Sat Oct 16, 2021 7:20 am We know that SSRIs cause it but bupropion/wellbutrin acts on dopamine/norepinephrine, not serotonin, unlike SSRIs.

And if bupropion can cause it, then why do dopamine agonists like pramipexole not cause it?

Something is missing here.

Edit:

I found an interesting comment on drugs.com

"David
August 11, 2018
“46 year old male. Started taking Bupropion (branded as Zyban) to help stop smoking. Unfortunately, within 1 day I completely lost the ability to o orgasm. I persisted once and 'forced' an orgasm. I immediately had an awful migraine-like headache. I suspect that those who find Bupropion helps their sex life, had low dopamine levels; Bupropion increases the effects of dopamine. For those like me, where Bupropion has killed their sex life, I suspect dopamine levels were already high - If you take a NDRI when you already have high dopamine levels, it will kill your libido/ability to orgasm, as the brain literally thinks you are always 'post-orgasm'! Orgasm is the point when the brain releases the most dopamine (narcotic drugs aside). If dopamine levels are too high, the brain thinks you have recently reached orgasm and will not allow you to orgasm (easily) to prevent very high dopamine levels, which can be harmful (can cause psychosis). This drug is certainly not for me.”
That part is true, but Wellbutrin also causes desensitization of the 5-HT1A receptors, like SSRI's.
Neuropharmacology
. 2008 Dec;55(7):1191-8. doi: 10.1016/j.neuropharm.2008.07.028. Epub 2008 Jul 30.
Sustained administration of bupropion alters the neuronal activity of serotonin, norepinephrine but not dopamine neurons in the rat brain
Mostafa El Mansari 1, Ramez Ghanbari, Shannon Janssen, Pierre Blier
Affiliations expand
PMID: 8708076 DOI: 10.1016/j.neuropharm.2008.07.028
Abstract
Bupropion is widely used in the treatment of depression. There are, however, limited data on its long-term effects on monoaminergic neurons and therefore the mechanism of its delayed onset of action is at present not well understood. The present study was conducted to examine the effects of prolonged bupropion administration on the firing activity of dorsal raphe nucleus (DRN), locus coeruleus (LC), and ventral tegmental area (VTA) neurons. Spontaneously firing neurons were recorded extracellularly in rats anesthetized with chloral hydrate. Bupropion (30 mg/kg/day) was administered using subcutaneously implanted minipumps. In the DRN, the firing rate of serotonin (5-HT) neurons was significantly increased after 2, 7 and 14 days of administration. The suppressant effect of LSD was significantly diminished after the two-day regimen, indicating a desensitization of 5-HT1A autoreceptors. In the LC, the firing rate of norepinephrine (NE) neurons was significantly attenuated after a 2-day regimen, but recovered progressively over 14 days of administration. The suppressant effect of clonidine on NE neuronal firing was significantly attenuated in rats treated with bupropion for 14 days, indicating a desensitization of alpha2-adrenoceptors. In the VTA, neither 2 nor 14 days of bupropion administration altered the firing and burst activity of dopamine neurons. These results indicate that bupropion, unlike 5-HT reuptake inhibitors, promptly increased 5-HT neuronal activity, due to early desensitization of the 5-HT1A autoreceptor. The gradual recovery of neuronal firing of NE neurons, due to the desensitization of alpha2-adrenoceptors, in the presence of the sustained increase in 5-HT neuronal firing, may explain in part the delayed onset of action of bupropion in major depression.
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