From 90mg adderall to 50mg vyvanse!!! WTF!

[Anxious.Individual]

I think it's worth mentioning that amphetamine is a quite a strong glutamate releasing agent, which is what causes memory loss during long term use, and it also explains why NMDA antagonists reduce amp tolerance, since they up regulate glutamate receptors. Methamphetamine on the other hand has no effect on glutamate, but has agonist action at sigma (both subtypes) / alpha-adrenergic receptors. So in the long run, methamphetamine is the healthier option.

Edit:
Also, meth's action on alpha receptors significantly reduces a lot of the cardiovascular strain, and lowers blood pressure.

 

[theGirlWithBlueHair]

It doesn't release glutamate. It potentiates calcium channels by releasing norepinephrine, which then causes subsequent glutamate release.

By action on alpha receptors, do you mean direct action?

EDIT:

yes, it does have agonistic activity on alpha, beta, and dopaminergic receptors:

http://www.ncbi.nlm.nih.gov/pubmed/1325059

 

[belligerent drunk]

^ I was under the impression that adrenergic receptor activation would lead to more cardiovascular strain (and increased BP), not the other way around. After all, beta adrenergic receptor blockers are used to lower blood pressure.

 

[theGirlWithBlueHair]

Not alpha 2 receptor actavation and it activation of dopamine D2 receptors is inhibitory and decreases cardiovascular strain as well. It doesn't mention its effect on beta adrenergic function



They antagonize it because they are more potent and they displace it - and this decreases cardiovascular effects as the beta 1 receptors are located in the heart.

This merely points out that it has affinity for the receptor, nothing more.

 

[Anxious.Individual]

It doesn't release glutamate. It potentiates calcium channels by releasing norepinephrine, which then causes subsequent glutamate release.

By action on alpha receptors, do you mean direct action?

EDIT:

yes, it does have agonistic activity on alpha, beta, and dopaminergic receptors:

http://www.ncbi.nlm.nih.gov/pubmed/1325059

Amp does release glutamate according to this: https://drugs-forum.com/forum/showthread.php?t=261785 (thread also contains sources)

EDIT: My bad, you're right, it indirectly increases glutamate release, but NOT through norepinephrine increase. However methamphetamine does not seem to have any effect on glutamate. Meth also appears to have agonist action at pre-synaptic 5HT-1A receptors and potentially at other 5-HT receptors.

 

[theGirlWithBlueHair]

Yes it does as norepinephrine activates calcium channels which release glutamate. This is a mechanism of action of indirectly releasing glutamate. It's fact.

Alpha 1 adrenergic agonists are sympathomimetic and are stimulanting; such as methoxamine, and phenylephrine (sudafed pe)

Alpha 1 antagonists are blood pressure medications ie prazosin (minipres) as they decrease calcium release, lowering norepinphrine (such as what verapamil does - a calcium channel blocker does) release, which also lowers glutamate with it.

 

[Built240]

I had the day off yesterday from not only work but the wife and kids so I decided to experiment with taking nothing. Not only did I feel awful but I slept about 16 hours and during the time I was up I needed a little bit of Xanax and only 5 mg oxy to combat the flu like aches I get from the amphetamine withdrawal. The day before yesterday, Friday I experimented with taking three times my normal vyvanse dose. During that day towards the end of the day I noticed I became extremely agitated(almost manic) and emotional. I really wish I could just figure out the right mix for what I need.

 

[belligerent drunk]

^ I think it is ill-advised to go days completely without your meds, and days with 3 x your usual dose. Assuming a 0.3-0.4 conversion rate, I believe two times 50 mg or maybe three times 50 mg would be optimal, but as always start low and work your way up.

 

[Built240]

I did 50 then a few hours 50 and a few hours later 50. Definitely never taking another day off again completely. I can't believe how lethargic and unfunctionalized was. I find it amazing when people say there are no physical symptoms from amphetamine withdrawal that is incorrect. I had extreme body aches and almost flulike feelings from just one day of being off of it.

 

[Built240]

Also something else I noticed was the day I took 150 mg vyvanse my heart rate was about 15points lower and blood pressure about 20points lower than days I take 80-90mg adderall

 

[AlphaMethylPhenyl]

Ho Chi Minh likes to be rude to people. He likes to take people's post and deconstruct them with his own blatant, misinformation that give readers incorrect ideas.

I was just telling you what my book stated

I will once again tell you how wrong you are about some things. If you're being combative because you're actually right, that's a lot different from what's going on now.

It's because dopamine is inhibitory at the D2 receptor. This is s an incredibly powerful inhibitory response. (Same channel as the GABA B receptor.) And norepinephrine decreases its own releases via its presynaptic alpha 2 receptors. Some people are very sensitive to these effects.

Where did you get that information? It couldn't be more wrong.

What does GABA B have anything to do with that?

All of the monoamines have autoreceptors. It's not some magic thing reserved for noradrenaline.

It means that when dopamine activates the D2 it produced a sedating response instead of a stimulating one. I don't think you are metabolizing it. When you start getting more dopamine released it starts activating the dopamine receptors on the presynaptic cells which shut off dopamine release which will cut off sedation.

You should dose however works best for you.

Again, wrong...is meth sedating?

It doesn't release glutamate. It potentiates calcium channels by releasing norepinephrine, which then causes subsequent glutamate release.

By action on alpha receptors, do you mean direct action?

EDIT:

yes, it does have agonistic activity on alpha, beta, and dopaminergic receptors:

http://www.ncbi.nlm.nih.gov/pubmed/1325059

Potentiates calcium channels?? How so?

If you want to be taken seriously, try finding a source that isn't 25 years old.

Yes it does as norepinephrine activates calcium channels which release glutamate. This is a mechanism of action of indirectly releasing glutamate. It's fact.

Alpha 1 adrenergic agonists are sympathomimetic and are stimulanting; such as methoxamine, and phenylephrine (sudafed pe)

Alpha 1 antagonists are blood pressure medications ie prazosin (minipres) as they decrease calcium release, lowering norepinphrine (such as what verapamil does - a calcium channel blocker does) release, which also lowers glutamate with it.

Do you know where calcium channels are located?

 

[theGirlWithBlueHair]

Calcium channels are located presynaptically

No. I said that when dopamine activates the D2 receptors, the D2 receptors is an inhibitory receptor. Not methamphetamine. The D1 receptror is stimulatory. Do you not connect the dots.


Pay better attention to what I say before You call me wrong. You are wrong. the D2 receptor IS inhibitory.

And yes, Norepinehphrine decreases it's own realease via alpha 2 receptors, look up the definition of autoreceptor.

It's because dopamine is inhibitory at the D2 receptor. This is s an incredibly powerful inhibitory response. (Same channel as the GABA B receptor.) And norepinephrine decreases its own releases via its presynaptic alpha 2 receptors. Some people are very sensitive to these effects

https://books.google.com/books?id=V5lg0aDSQnIC&pg=PT18&lpg=PT18&dq=GABA+B+D2+GIRK+CHANNEL&source=bl&ots=9gye3c0Lka&sig=7NRa_9IosTaJ2UJSfutmbPcOiGk&hl=en&sa=X&ved=0ahUKEwig6NT249zNAhXKHx4KHdB1BacQ6AEIZjAJ#v=onepage&q=GABA%20B%20D2%20GIRK%20CHANNEL&f=false

This is what I meant to say. Otherwise it is all true.

 

[theGirlWithBlueHair]

I will once again tell you how wrong you are about some things. If you're being combative because you're actually right, that's a lot different from what's going on now.



Where did you get that information? It couldn't be more wrong.

What does GABA B have anything to do with that?

All of the monoamines have autoreceptors. It's not some magic thing reserved for noradrenaline.



Again, wrong...is meth sedating?



Potentiates calcium channels?? How so?

If you want to be taken seriously, try finding a source that isn't 25 years old.



Do you know where calcium channels are located?

Potentiates calcium channels by releasing norepinephrine which then activates alpha receptors which release calcium...?

 

[theGirlWithBlueHair]

Something that's been proven scientifically in vivo​ doesn't need a newer source. That will suffice.

 

[theGirlWithBlueHair]

>Again, wrong...is meth sedating?

No. I was simply pointing out that methamphetamine has inhibitory mechanisms that counteract its stimulating ones, which is why it provides a more euphoric feeling to more "speedy" racemic amphetamine...

I consistently always need to countercorrect everything you feel the need to "correct" in my posts...

 

[AlphaMethylPhenyl]

Calcium channels are located presynaptically

No. I said that when dopamine activates the D2 receptors, the D2 receptors is an inhibitory receptor. Not methamphetamine. The D1 receptror is stimulatory. Do you not connect the dots.


Pay better attention to what I say before You call me wrong. You are wrong. the D2 receptor IS inhibitory.

And yes, Norepinehphrine decreases it's own realease via alpha 2 receptors, look up the definition of autoreceptor.

It's because dopamine is inhibitory at the D2 receptor. This is s an incredibly powerful inhibitory response. (Same channel as the GABA B receptor.) And norepinephrine decreases its own releases via its presynaptic alpha 2 receptors. Some people are very sensitive to these effects

https://books.google.com/books?id=V5lg0aDSQnIC&pg=PT18&lpg=PT18&dq=GABA+B+D2+GIRK+CHANNEL&source=bl&ots=9gye3c0Lka&sig=7NRa_9IosTaJ2UJSfutmbPcOiGk&hl=en&sa=X&ved=0ahUKEwig6NT249zNAhXKHx4KHdB1BacQ6AEIZjAJ#v=onepage&q=GABA%20B%20D2%20GIRK%20CHANNEL&f=false

This is what I meant to say. Otherwise it is all true.

Are you serious? If meth somehow selectively leads to more activity at D1, there would be little reward, and many fewer cases of psychosis. You do understand that almost all antipsychotics are D2 antagonists, right? And that the main explanation for decreasing positive symptoms is the D2 antagonism? I don't connect dots. I understand systems.

I could swear you're trolling.

Potentiates calcium channels by releasing norepinephrine which then activates alpha receptors which release calcium...?

...?

Something that's been proven scientifically in vivo​ doesn't need a newer source. That will suffice.

Except for the fact that we don't kill people to conduct experiments. Maybe you didn't know that?

http://www.sciencemag.org/news/2016/01/more-details-emerge-fateful-french-drug-trial

I rest my case

>Again, wrong...is meth sedating?

No. I was simply pointing out that methamphetamine has inhibitory mechanisms that counteract its stimulating ones, which is why it provides a more euphoric feeling to more "speedy" racemic amphetamine...

I consistently always need to countercorrect everything you feel the need to "correct" in my posts...

That's the most stupid thing I've ever...sorry. It's kind of funny actually.

 

[theGirlWithBlueHair]

I'm just saying that the D2 is inhibitory, which you seem to be denying?

I meant to say in vitro. They prove it in vitro.

 

[theGirlWithBlueHair]

Trolling my ass. You said the D2 receptor is inhibitory. IT IS. And I NEVER said meth was selective for anything. I swear you do not even read, but merely, skim my posts sometimes.

 

[theGirlWithBlueHair]

If haloperidol counteracted cardiovascular effects of methamphetamine it means methamphetamine BINDS to the D2 receptors. D2 ligands LOWER BLOOD PRESSURE AND PULSE RATE

ie pramipexole or ropinirole. They are sedatives and cause hypotension and sleep attacks. They are GIRK channels and blocking them prevents potassium from entering the cell, causing DEPOLARIZATION.

 

[Built240]

If haloperidol counteracted cardiovascular effects of methamphetamine it means methamphetamine BINDS to the D2 receptors. D2 ligands LOWER BLOOD PRESSURE AND PULSE RATE

ie pramipexole or ropinirole. They are sedatives and cause hypotension and sleep attacks. They are GIRK channels and blocking them prevents potassium from entering the cell, causing DEPOLARIZATION.

Interesting. Us bodybuilders use pramipexole and/or cabergoline to counter act the negative side effects of prolactin that certain steroids cause.