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  • BDD Moderators: Keif’ Richards | negrogesic

Mirtazapine blocks dopamine?

S

Stanfoo

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Joined
Jul 20, 2019
Messages
7
Saw this post: "Mirtazapine antagonizes the 5-HT2c receptor (especially at higher doses 45-90mg), which has been discovered to regulate and actually block dopamine and noradrenaline activity in many parts of the brain; especially the pleasure centers. "

Does it actually block dopamine? That'd be bad.
 
Not really?? Its a medication used for sleep, blocking dopamine is effective for that.
 
Stanfoo said:
Saw this post: "Mirtazapine antagonizes the 5-HT2c receptor (especially at higher doses 45-90mg), which has been discovered to regulate and actually block dopamine and noradrenaline activity in many parts of the brain; especially the pleasure centers. "

Does it actually block dopamine? That'd be bad.
Click to expand...

How so ?

"Roads" goes on to state in 9b) Antagonism of the 5-HT2c serotonin receptor results in a disinhibition of that dopamine in the nucleus accumbens, ventral tegmental area and other parts of the mesolimbic and mesocorticol reward pathways. This leads Mirtazapine to produce more stimulant effects the higher the dosage used; especially after histamine receptors down regulate following a few weeks of daily administration. SWIM no longer takes his Remeron at night, but in the morning due to this exact reason. SWIM almost always gets a nice "head buzz" for a few hours after taking Remeron. The increased dopamine production/release in the reward pathways may help explain the mild euphoric properties; especially in high doses (90-120mg+).

Dopamine in the Nucleus Accumbens and the Ventral striatal zone serve to fulfill reward seeking and to prevent apathy, Abulia, Anergia, depression and anxiety. The Caudate acts as the Brains " Gear shifter" to the Orbito Pre-frontal cortex and then back to regulate/modulate through the Caudate > Putamen> Globus Pallidus and then to other areas of need. This is the Frontal Striatal circuit, which is largely innervated with Dopamine, originating from the Substantia Nigra proper.

9a) probably was copied or presented Incorrectly , as was most likely intended to read as " To Block RE-UPTAKE of Dopamnine and Norepinephrine" meaning there's a more steady and abundant supply.

See down further he states :

Furthermore, the aforementioned blockade of 5-HT2c serotonin receptors disinhibits dopamine in the most important cerebral parts to us SWIMmers: The Mesolimbic dopamine pathway. The pleasure center baby! SWIM theorizes that this disinhibition allows amphetamine to not only have access to more stores of dopamine, but to allow it to release more and at a higher rate when it does open those depots.

Disinhibits means does not Inhibit or Block!

101- Keep in mind his post is regarding his Hypothesis that adding Mirtazapine can potentiate his Stimulant Medication.
 
karambit said:
How so ?

"Roads" goes on to state in 9b) Antagonism of the 5-HT2c serotonin receptor results in a disinhibition of that dopamine in the nucleus accumbens, ventral tegmental area and other parts of the mesolimbic and mesocorticol reward pathways. This leads Mirtazapine to produce more stimulant effects the higher the dosage used; especially after histamine receptors down regulate following a few weeks of daily administration. SWIM no longer takes his Remeron at night, but in the morning due to this exact reason. SWIM almost always gets a nice "head buzz" for a few hours after taking Remeron. The increased dopamine production/release in the reward pathways may help explain the mild euphoric properties; especially in high doses (90-120mg+).

Dopamine in the Nucleus Accumbens and the Ventral striatal zone serve to fulfill reward seeking and to prevent apathy, Abulia, Anergia, depression and anxiety. The Caudate acts as the Brains " Gear shifter" to the Orbito Pre-frontal cortex and then back to regulate/modulate through the Caudate > Putamen> Globus Pallidus and then to other areas of need. This is the Frontal Striatal circuit, which is largely innervated with Dopamine, originating from the Substantia Nigra proper.

9a) probably was copied or presented Incorrectly , as was most likely intended to read as " To Block RE-UPTAKE of Dopamnine and Norepinephrine" meaning there's a more steady and abundant supply.

See down further he states :

Furthermore, the aforementioned blockade of 5-HT2c serotonin receptors disinhibits dopamine in the most important cerebral parts to us SWIMmers: The Mesolimbic dopamine pathway. The pleasure center baby! SWIM theorizes that this disinhibition allows amphetamine to not only have access to more stores of dopamine, but to allow it to release more and at a higher rate when it does open those depots.

Disinhibits means does not Inhibit or Block!

101- Keep in mind his post is regarding his Hypothesis that adding Mirtazapine can potentiate his Stimulant Medication.
Click to expand...
If it blocks dopamine he's either full of shit or hasnt a clue what hes talking about. Dopamine causes alertness, pleasure and a few of the aboves, take cocaine for example, its main and almost only function is to prevent reuptake of dopamine letting it build up causing euphoria, stimulation, and alertness. Thus doing the opposite would have opposite effects.
 
www.ncbi.nlm.nih.gov

5-HT2A and 5-HT2C receptors and their atypical regulation properties - PubMed

The 5-HT(2A) and 5-HT(2C) receptors belong to the G-protein-coupled receptor (GPCR) superfamily. GPCRs transduce extracellular signals to the interior of cells through their interaction with G-proteins. The 5-HT(2A) and 5-HT(2C) receptors mediate effects of a large variety of compounds affecting...
www.ncbi.nlm.nih.gov www.ncbi.nlm.nih.gov

Antagonism of 5 ht2c receptors may result in paradoxical downregulation of 5 ht2c receptors.

Therefore, i would assume that yes short term 5ht2c antagonism might have some effect on increasing dopamine. However, the larger effect is possibly by taking it long term like ssris (indirect sert blockade increasing seritonin increasing 5 ht2c activation causing downregulation) partly by downregulation of 5ht2c receptors.

I believe this long term down regulation is likely more relevant because it more closely fits in line with the antidepressants efficacy. Rather than working instantly. Also, that a ssri + 5 ht2a/c antagonist may speed up the time till antidepressant response.
 
I disagree that Mirtazapine causes stimulation at higher doses (or any dose for that matter). I took Mirtazapine for 2 years and the higher the dose I took the more sedating it was. I also found Mirtazapine to be effective at negating the effects of Cocaine which suggests it has some sort of antagonizing effect on dopamine.
 
the effects of specific neurotransmitters are often over generalized. they do wildly different things in different areas of the brain and often have major cascading effects.

my knowledge is very undergrad as well, but it’s safe to assume anything saying “pleasure center” is an oversimplification. like learning what a neuron looks like only to later learn none of them actually look anything like that. the simplification allowed you to develop an understanding of the structure, but was also misleading when extrapolated.
 
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I take mirtazipine and haven't noticed any dopamine depletion. It has helped with paws, i sleep a bit better and i find im not as anxious anymore.
I still laugh and have fun, actually i do that more now then when i was on drugs.
I don't know anything about the pharmacology of this drug though, just how i felt before and after
 
I liked Mirtazapine when I was prescribed it, it had next to no side-effects and it was ALOT more tolerable than SSRIs/SNRIs. It was great for getting me to sleep at night and the anti-depressant effects were good too.

EDIT: The only side-effect I got was increased appetite but it was welcome as I was under weight at the time. I enjoyed my food a lot more!
 
I'd say yes. Chemically, it is VERY similar to Quetiapine and Olanzapine and they both significantly block dopamine.
Like the two drugs, it also increases your need for sleep and massively stimulates your appetite. They give Mirtazapine to does who won't eat.
 
My understanding was that mirtazepine has some dopamine reducing activity specifically in the nucleus accumblens, often thought to be a pleasure centre of the brain that drugs hit... for that reason, and maybe some kappa opioid effect, some doctors have thought mirtazepine could be useful to reduce drug seeking behaviour. It's probably the same mechanism which leads to weight gain or decreased satiety after eating.
 
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