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Strattera As A Wellbutrin Alternative


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#1 j03

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Posted 25 January 2010 - 05:37 AM


I was using Wellbutrin for awhile and I was feeling fantastic on it! It almost immediately turned my world into sunshine and rainbows. However, it severely limited my short term memory. It made me feel like I was straining to think and it was terribly uncomfortable, so i had to stop even though i really liked the positive effects from it.

Guanfacine isn't available in my area, and stims like Ritalin, modofinal, etc. made me feel like Wellbutrin did except I couldn't sleep and had impotence issue on it. So, I came across Strattera as a norepinephrine reuptake inhibitor, and possible substitute. I'm thinking about taking Strattera with tyrosine and that might make me feel the same.

Is this the best option? any other recommendations?

Thanks in advance.

#2 Pike

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Posted 25 January 2010 - 01:06 PM

i've never touched the stuff, however, every single person i've ever met with ADHD who took strattera hated it with a firey passion and never even got past a week before they changed their prescription. as i understand, the "curve" so to speak before any of the initial side effects subside is a full straight month, after which, the side effects just become less noticeable. After all of the ADHD forums i've gone through, and all the ADDers i've met, not one has had anything good to say about strattera.

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#3 FunkOdyssey

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Posted 25 January 2010 - 04:45 PM

Guanfacine isn't available in my area, and stims like Ritalin, modofinal, etc. made me feel like Wellbutrin did except I couldn't sleep and had impotence issue on it.


Strattera is almost universally disliked by patients and has an array of serious/bizarre side effects. Have you tried focalin? Its a single isomer version of ritalin that is less peripherally stimulating and would be less apt to cause the insomnia/impotence you experienced before.

#4 tlm884

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Posted 26 January 2010 - 02:51 AM

I was using Wellbutrin for awhile and I was feeling fantastic on it! It almost immediately turned my world into sunshine and rainbows. However, it severely limited my short term memory. It made me feel like I was straining to think and it was terribly uncomfortable, so i had to stop even though i really liked the positive effects from it.

Guanfacine isn't available in my area, and stims like Ritalin, modofinal, etc. made me feel like Wellbutrin did except I couldn't sleep and had impotence issue on it. So, I came across Strattera as a norepinephrine reuptake inhibitor, and possible substitute. I'm thinking about taking Strattera with tyrosine and that might make me feel the same.

Is this the best option? any other recommendations?

Thanks in advance.


I was on Straterra for about 5 months. It did nothing for my concentration, gave me horrible insomnia, and trashed my liver. It attributed highly to my fatty liver. Wellbutrin is by FAR better then Straterra and I am so glad to be back on it. If you must try an SNRI I would try Pristiq or its older version Effexor. However, do some research on other things that may be causing the memory problems.

#5 j03

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Posted 26 January 2010 - 04:41 AM

Wow the consensus seems to quite negative for this drug

FunkOdyssey: focalin looks like an interesting drug! But unfortunately it isn't available in my area. This seems to happen with every interesting drug i want to try. I might look into finding a reputable source or driving across the border and trying to get it that way. i would be interested in that and guanfacine.

tlm884: I agree Wellbutrin was a good drug, but the cognitive side effects for me were too much. And any drugs that play around with serotonin (including even St. Johns wort) seem to cause me bruxism... they also don't do much in terms of mood, so this is why I was focused on dopamine and norepinephrine

Edited by k4t, 26 January 2010 - 04:42 AM.


#6 SE102

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Posted 27 January 2010 - 03:35 AM

I take strattera currently as an alternative to ritalin/adderal.
I would say it works well I feel no stimulating effect yet functional and organized with a little effort.

As for the side effects, I experience none. I take it going through Geodon's onslaught of side effects has made me immune to them ;)

stoopid Geodong...

#7 bluebird2

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Posted 28 January 2010 - 02:10 AM

I take strattera currently as an alternative to ritalin/adderal.
I would say it works well I feel no stimulating effect yet functional and organized with a little effort.

As for the side effects, I experience none. I take it going through Geodon's onslaught of side effects has made me immune to them :-D

stoopid Geodong...


On the subject of side effects, in one study almost 2% of those who used strattera became suicidal. And over long term use, an additional 2% had appendicitis. Not the best medication but does have its uses, which may as other posters have noted, be limited by the coming of intuniv

source: strattera: side effects, use

#8 alexd

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Posted 28 January 2010 - 04:03 PM

Strattera worked well for me but modafinal works better.

#9 luv2increase

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Posted 29 January 2010 - 07:36 AM

I thought the same thing about tramadol when I first starting taking it. I thought the world was awesome, and life was great. Then, I realized how stupid it made me and negated any of the positive effects of my nootropics. :(

Any SSRI/SNRI will make you feel this way --> happy yet dumb

#10 KimberCT

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Posted 29 January 2010 - 12:28 PM

All 20mg of Strattera did for me was make me tired, anxious, and give me a two day headache.

#11 navyblue

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Posted 30 January 2010 - 09:32 AM

Was on Strattera for 3 months. 25mg for 1 1/2 months, then 40mg for 1 1/2 months. Side effects: just plain felt weird. Awkward sleep pattern and many more. It help a little with concentration and energy, but did absolutely nothing for motivation, and organizational abilities.

Have you tried focalin? Its a single isomer version of ritalin that is less peripherally stimulating and would be less apt to cause the insomnia/impotence you experienced before.


Thanks Funk for the recommendation to the original poster. I myself might give this a chance as Ritalin made me too agitated the last time I tried it.

Bottom Line: In my opinion Strattera is just not worth it. There are better combination out there, you just have to find the right one which of course is easier said than done.

#12 ultranaut

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Posted 02 February 2010 - 04:01 AM

I was on Straterra, briefly like most. By far the worst drug I've ever taken, I'm amazed that stuff is legal. I was already on Wellbutrin, Straterra was my first treatment for ADD. Ultimately I found my way to Adderal. It's great stuff, I haven't renewed my prescription recently so it's been awhile since I've taken any. It's the kind of drug that taking a break from is probably a good idea on occasion. I'll probably do that soon though, if I remember. I still take Wellbutrin regularly, I think it probably has had some minor effects on my short-term memory but they are worth it to me. There is nothing wrong with being a little absent-minded. If I ever really need to be sharp the Adderal is there. I think Wellbutrin has also had some cognitive benefits, I was a terrible Scrabble player before I started taking it...

#13 demitriden

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Posted 02 February 2010 - 04:15 AM

I'm on Wellbutrin as well. Initially I was prescribed that to combat sexual side-effects from Paxil. I was given the lowest dose of Wellbutrin of 150 XL and it was still immensely magnificent in many ways. Mood, motivation, was great. The best part was that it took care of my fibromalygia! Something that was very unexpected. Anyway, after I while I realized that I began to suffer from some really bad cognitive side-effects from Wellbutrin. My typo errors have increased EXPONTENTIALLY, and I have a very hard time recalling items from my short-term or working memory (not sure exactly which yet).. but I think working memory. Anyway, I'm going to go back and ask for another drug. From extensive research, I'll probably go with Remeron or Cymbalta.

#14 ultranaut

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Posted 04 February 2010 - 04:50 AM

Anyway, after I while I realized that I began to suffer from some really bad cognitive side-effects from Wellbutrin. My typo errors have increased EXPONTENTIALLY, and I have a very hard time recalling items from my short-term or working memory (not sure exactly which yet).. but I think working memory.


I noticed the same thing with typos increasing. I think a lot of it comes from excessive multitasking. I find myself working on more things at once, unless I take Adderal or something similar. I know some people have ADD symptoms decreased from Wellbutrin but in my case I think it has a slight opposite effect.

#15 SubMerged

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Posted 05 February 2010 - 11:17 AM

strattera made me feel great - i would even call it euphoric - it also has a low side effect profile compared to SSRIs.

you guys need more patience - it does make you feel wonky for a few days as you get used to it, but after that, it's smooth sailing. also, make sure you start on the right dosage - a seemingly high number of people start off too high (from 40-60) when they should be gradually coming up from 25 - receiving too high a dose actually does the opposite of what strattera is supposed to do and depletes norepinephrine. it's happened to me when i mixed dosages - a truely shitty feeling indeed. taking l-tyrosine with it is a good idea to make more norepinephrine available.

read this: http://www.crazymeds.us/strattera.html

#16 sameer_hasham

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Posted 21 May 2010 - 04:30 PM

i too would like to find an alternative to Wellbutrin, but for different reasons. It gave me really bad constipation. I think this is becasue it works (in addition to a DA NE reuptake inhibitor) as a α3β4-nicotinic receptor antagonist. This playes havoc with my peristalsis. Ie. musles dont push crap through the gut.

anyway, wellbutrin worked wonders for me; i felt truely alive - and i was learning things and getting on with whatever i wanted to do. i wish i wish i wish i could take it again, but i'm worried about the constipation ( i have ibs-c )

thanks to who ever it is that mentioned Focalin. it could work like wellbutrin as it is a DA and NE reuptake inhibitor (ie it allows already present DA and NE to stick around for a while) as opposed to most stimulants that push new DA and NE (if i'm not mistaken)

k42 and others - have you tried Focalin ??

#17 dilenja

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Posted 21 May 2010 - 06:21 PM

Straterra seems to be better tolerated by those with inattentive ADD (I-ADD) than by those with primarily ADHD or the combined type. The reason for this would seem to be that Straterra does not alter DA in the striatum, which is considered to be the area most associated with ADHD and combined ADHD (but not in I-ADD; Prefrontal Cortex)

The Dopamine 4 (D4) receptor is implicated in I-ADD and is considered a catecholamine rather than strictly a dopamine receptor, which means it has affinity for nor-epinephrine in addition to dopamine. Since Straterra increases NE and Dopamine in the prefrontal cortex (which is rich with D4 receptors), but not in the striatum, this could perhaps explain part of the reason why individuals have reported mixed results.



i too would like to find an alternative to Wellbutrin, but for different reasons. It gave me really bad constipation. I think this is becasue it works (in addition to a DA NE reuptake inhibitor) as a α3β4-nicotinic receptor antagonist. This playes havoc with my peristalsis. Ie. musles dont push crap through the gut.

anyway, wellbutrin worked wonders for me; i felt truely alive - and i was learning things and getting on with whatever i wanted to do. i wish i wish i wish i could take it again, but i'm worried about the constipation ( i have ibs-c )

thanks to who ever it is that mentioned Focalin. it could work like wellbutrin as it is a DA and NE reuptake inhibitor (ie it allows already present DA and NE to stick around for a while) as opposed to most stimulants that push new DA and NE (if i'm not mistaken)

k42 and others - have you tried Focalin ??



#18 Mind_Paralysis

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Posted 24 July 2016 - 11:40 AM

Straterra seems to be better tolerated by those with inattentive ADD (I-ADD) than by those with primarily ADHD or the combined type. The reason for this would seem to be that Straterra does not alter DA in the striatum, which is considered to be the area most associated with ADHD and combined ADHD (but not in I-ADD; Prefrontal Cortex)

The Dopamine 4 (D4) receptor is implicated in I-ADD and is considered a catecholamine rather than strictly a dopamine receptor, which means it has affinity for nor-epinephrine in addition to dopamine. Since Straterra increases NE and Dopamine in the prefrontal cortex (which is rich with D4 receptors), but not in the striatum, this could perhaps explain part of the reason why individuals have reported mixed results.

 

 


 

 

Fascinating! I had NO idea that the D4-receptor is actually responsive to Norepinephrine as well! : O Do you mind showing a link? I need to know more about this...

 

I'm currently trying Wellbutrin as an alternative to Strattera - and I know the anticholinergic memory-effect you mention - I had it extensively the last time I took it as well. I'm currently using nicotine gum, as an experimental way of clearing some of that effect away - not entirely sure about the results yet... But I will report back soon with my experiences.



#19 jack black

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Posted 24 July 2016 - 12:32 PM

Shouldn't anti cholinergic effect fade in a few days due to receptor upregulation? This is what happens with memantine that I'm taking now. Worsening dyslexia initially but not noticeable a week later.

#20 Mind_Paralysis

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Posted 24 July 2016 - 02:50 PM

Shouldn't anti cholinergic effect fade in a few days due to receptor upregulation? This is what happens with memantine that I'm taking now. Worsening dyslexia initially but not noticeable a week later.

 

Well, it depends on the mechanism, strength of said mechanism, and the biological curiosities of the subject in question - not everyone experiences the anticholinergic side-effects of Wellbutrin at all - yet some, like me, seems to be continously susceptible to it.

 

Perhaps we have a permanent overplethora of Cholinergic receptors? In my case, I have genes controlling nicotinic receptors which proposes that I am more likely to become dependent. Maybe part of that is because I have some mechanism in me which prevents receptor up and deregulation to some extent?

 

There is a high variability to susceptibility to these side-effects - and most people don't even seem to notice the anticholinergic effects - so they must obviously have highly differing receptors from those that do.

 

There is actually, shockingly enough, people that can use even GABA-ergics like Benzo's for years on end, without any seemingly greater loss of efficacy.

 

 

I actually dug up some interesting studies on tolerance to Benzodiazepines - the tolerance-developing "standard" of medicine, if you like.

 

Mechanisms Underlying Tolerance after Long-Term Benzodiazepine Use: A Future for Subtype-Selective Receptor Modulators?

http://www.hindawi.c...ps/2012/416864/

 

It seems like tolerance does not develop the same way in receptors that are affected by the same neurotransmitters even - rather interesting fact, because it makes the resistance of the D4-receptors to up and de-regulation no longer seem like such an unusual feature - there are other receptors with this behaviour as well.

Ey, I even found an article regarding resistance towards down-regulation of GABA-receptors! Check it out. I am going to assume that a similar mechanism may be involved in those of us that don't experience any greater anticholinergic tolerance - I'm guessing it's specifically one of the nicotinic subunits - since I actually did develop tolerance to the hypnotic effects of Promethazine (lergigan) to some extent. (still had god-awful hangover the next day, it just didn't put me to sleep. Which implies that some of the anticholinergic effects remained)
 

Figure 5: siRNA-resistant GABAB2 rescues phenotypes associated with wild-type GABAB2-subunit downregulation.

http://www.nature.co...mms2820_F5.html


Edited by Stinkorninjor, 24 July 2016 - 02:53 PM.


#21 Finn

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Posted 25 July 2016 - 10:23 AM

 

Straterra seems to be better tolerated by those with inattentive ADD (I-ADD) than by those with primarily ADHD or the combined type. The reason for this would seem to be that Straterra does not alter DA in the striatum, which is considered to be the area most associated with ADHD and combined ADHD (but not in I-ADD; Prefrontal Cortex)

The Dopamine 4 (D4) receptor is implicated in I-ADD and is considered a catecholamine rather than strictly a dopamine receptor, which means it has affinity for nor-epinephrine in addition to dopamine. Since Straterra increases NE and Dopamine in the prefrontal cortex (which is rich with D4 receptors), but not in the striatum, this could perhaps explain part of the reason why individuals have reported mixed results.

 

 


 

 

Fascinating! I had NO idea that the D4-receptor is actually responsive to Norepinephrine as well! : O Do you mind showing a link? I need to know more about this...

 

I'm currently trying Wellbutrin as an alternative to Strattera - and I know the anticholinergic memory-effect you mention - I had it extensively the last time I took it as well. I'm currently using nicotine gum, as an experimental way of clearing some of that effect away - not entirely sure about the results yet... But I will report back soon with my experiences.

 

http://www.sciencedi...014299996009855

 

 
Noradrenaline and adrenaline are high affinity agonists at dopamine D4 receptors

 

Abstract

The activity of monoamine neurotransmitters was examined at dopamine D4 receptors. In competition binding with [3H]spiperone, noradrenaline and adrenaline exhibited a high affinity binding component (KH=12.1 nM and 5.0 nM ,respectively), similar to that of dopamine (KH=2.6 nM), whereas serotonin (5-hydroxytryptamine, 5-HT) and histamine had low affinity (Ki>1000 nM). Noradrenaline and adrenaline acted as agonists at dopamine D4 receptors, stimulating receptor-mediated [35S]guanylyl-γ-thiotriphosphate ([35S]GTPγS) binding (EC50=7.8 and 5.8 μM, respectively, versus 0.1 μM for dopamine). The dopamine D4 receptor-selective ligand, 3-(4-[4-chlorophenyl]piperazin-1-yl)methyl-1H-pyrrolo[2,3b]-pyridine (L 745,870) and the dopaminergic antagonists, spiperone, haloperidol and clozapine, inhibited noradrenaline-stimulated [35S]GTPγS binding whereas α1-, α2- and β-adrenoceptor antagonists did not. These results indicate that dopamine D4 receptors are activated by noradrenaline and adrenaline, although at 50–100-fold higher concentrations than dopamine.

 

 



#22 Mind_Paralysis

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Posted 25 July 2016 - 11:31 AM

 

 

Straterra seems to be better tolerated by those with inattentive ADD (I-ADD) than by those with primarily ADHD or the combined type. The reason for this would seem to be that Straterra does not alter DA in the striatum, which is considered to be the area most associated with ADHD and combined ADHD (but not in I-ADD; Prefrontal Cortex)

The Dopamine 4 (D4) receptor is implicated in I-ADD and is considered a catecholamine rather than strictly a dopamine receptor, which means it has affinity for nor-epinephrine in addition to dopamine. Since Straterra increases NE and Dopamine in the prefrontal cortex (which is rich with D4 receptors), but not in the striatum, this could perhaps explain part of the reason why individuals have reported mixed results.

 

 


 

 

Fascinating! I had NO idea that the D4-receptor is actually responsive to Norepinephrine as well! : O Do you mind showing a link? I need to know more about this...

 

I'm currently trying Wellbutrin as an alternative to Strattera - and I know the anticholinergic memory-effect you mention - I had it extensively the last time I took it as well. I'm currently using nicotine gum, as an experimental way of clearing some of that effect away - not entirely sure about the results yet... But I will report back soon with my experiences.

 

http://www.sciencedi...014299996009855

 

 
Noradrenaline and adrenaline are high affinity agonists at dopamine D4 receptors

 

Abstract

The activity of monoamine neurotransmitters was examined at dopamine D4 receptors. In competition binding with [3H]spiperone, noradrenaline and adrenaline exhibited a high affinity binding component (KH=12.1 nM and 5.0 nM ,respectively), similar to that of dopamine (KH=2.6 nM), whereas serotonin (5-hydroxytryptamine, 5-HT) and histamine had low affinity (Ki>1000 nM). Noradrenaline and adrenaline acted as agonists at dopamine D4 receptors, stimulating receptor-mediated [35S]guanylyl-γ-thiotriphosphate ([35S]GTPγS) binding (EC50=7.8 and 5.8 μM, respectively, versus 0.1 μM for dopamine). The dopamine D4 receptor-selective ligand, 3-(4-[4-chlorophenyl]piperazin-1-yl)methyl-1H-pyrrolo[2,3b]-pyridine (L 745,870) and the dopaminergic antagonists, spiperone, haloperidol and clozapine, inhibited noradrenaline-stimulated [35S]GTPγS binding whereas α1-, α2- and β-adrenoceptor antagonists did not. These results indicate that dopamine D4 receptors are activated by noradrenaline and adrenaline, although at 50–100-fold higher concentrations than dopamine.

 

 

 

 

Cheers for the link, mate.

 

Well, that's another possible explanation of why SCT-ers need extreme stress to work consistently, since it would stand to reason that Adrenaline-levels are increased at such times, and only when they achieve a high enough level, they will start knocking the D4-receptors enough to achieve therapeutic effect.

 

Ey, Finn - what's your take on this in relation to the recent finding that dopamine and norepinephrine release in the PFC is controlled by glucocorticoids? How would they relate to each other, and to the hypothesis that D4-receptors are impaired in SCT?

EDIT:

Oh! Just realized that this is proof that at sufficient levels, Strattera would be beneficial to those with impaired D4-receptors as well! It certainly makes it seem like the right drug with that in mind...


Edited by Stinkorninjor, 25 July 2016 - 11:33 AM.


#23 Heinsbeans

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Posted 05 April 2020 - 07:23 AM

Cheers for the link, mate.

 

Well, that's another possible explanation of why SCT-ers need extreme stress to work consistently, since it would stand to reason that Adrenaline-levels are increased at such times, and only when they achieve a high enough level, they will start knocking the D4-receptors enough to achieve therapeutic effect.

 

Ey, Finn - what's your take on this in relation to the recent finding that dopamine and norepinephrine release in the PFC is controlled by glucocorticoids? How would they relate to each other, and to the hypothesis that D4-receptors are impaired in SCT?

EDIT:

Oh! Just realized that this is proof that at sufficient levels, Strattera would be beneficial to those with impaired D4-receptors as well! It certainly makes it seem like the right drug with that in mind...


Strattera is a kappa-opioid partial agonist, which induces stress response. So that could well be why it helps with procrastination symptoms that requires the activation of a stressor. Like for example, when I'm procrastinating on my assignments, I typically don't start doing them until it's too late which induces stress response in me and I find myself doing my assignment with ease without hesitation:

Although the mechanism most attributed to atomoxetine’s therapeutic benefit in the treatment of ADHD is its role as a highly selective norepinephrine transport inhibitor, Creighton et al.3 discussed the role of the 4-hydroxyatomoxetine, the human metabolite of atomoxetine, as a partial kappa-opioid receptor (KOR) agonist. Studies are increasingly suggesting that activation of the KORs is involved in the stress response


Atomoxetine, ADHD, and the ongoing debate about increased risk of suicidal behaviors: the understudied role of kappa opioid receptor agonism: https://pubmed.ncbi....h.gov/27283209/
Synthesis and Biological Evaluation of the Major Metabolite of Atomoxetine: Elucidation of a Partial Kappa-Opioid Agonist Effect: https://pubmed.ncbi....h.gov/15225731/


But this is the worrying part about atomoxetine, which is that it potentially has pro-depressant properties. Due to that kappa-opioid partial agonism:

Positive modulation of the hypothalamic pituitary adrenal (HPA) axis (defined by plasma corticosterone levels) by systemic administration of kappa opioid agonists has been shown in rat,5 suggesting activation of KOR may induce systemic hormonal changes indicative of its pro- depressant properties. However, KOR agonism and induction of HPA activity are mechanisms of action that are rarely considered in pharmacovigilance studies assessing the link between atomoxetine use and suicidal risk, even though HPA hyperactivity has been implicated in suicidal behavior.


Sedation of atomoxetine by the way, is also probably caused by its kappa-opioid partial agonism as well. Rather than from the uncompetitive NMDA antagonism that also occurs at clinically relevant dose. There seems to be nothing good coming out of activating this receptor.


Edited by Heinsbeans, 05 April 2020 - 07:37 AM.


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#24 gamesguru

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Posted 07 April 2020 - 04:56 PM

Strattera is a kappa-opioid partial agonist, which induces stress response. So that could well be why it helps with procrastination symptoms that requires the activation of a stressor. Like for example, when I'm procrastinating on my assignments, I typically don't start doing them until it's too late which induces stress response in me and I find myself doing my assignment with ease without hesitation:

 

Strattera definitely has some utility in ADHD, but it's not the first choice.  It's also not seen much success in childhood ADHD.

 

I think dopamine and norepinephrine have a bigger role here, however, than cortisol.  Stress is a poor motivator: it is a reaction rather than a proactive choice.

 

Science. 2020 Mar 20;367(6484):1362-1366. doi: 10.1126/science.aaz5891.
 
Dopamine promotes cognitive effort by biasing the benefits versus costs of cognitive work

Stimulants such as methylphenidate are increasingly used for cognitive enhancement but precise mechanisms are unknown. We found that methylphenidate boosts willingness to expend cognitive effort by altering the benefit-to-cost ratio of cognitive work. Willingness to expend effort was greater for participants with higher striatal dopamine synthesis capacity, whereas methylphenidate and sulpiride, a selective D2 receptor antagonist, increased cognitive motivation more for participants with lower synthesis capacity. A sequential sampling model informed by momentary gaze revealed that decisions to expend effort are related to amplification of benefit-versus-cost information attended early in the decision process, whereas the effect of benefits is strengthened with higher synthesis capacity and by methylphenidate. These findings demonstrate that methylphenidate boosts the perceived benefits versus costs of cognitive effort by modulating striatal dopamine signaling.


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