i just want to know what is recommended, i understand that for many these stimulants come with many negatives, is amp the best option for study aid/cognitive enhancer?
i just want to know what is recommended, i understand that for many these stimulants come with many negatives, is amp the best option for study aid/cognitive enhancer?
Amphetamine or modafinil. Depends on the individual.Originally Posted by rovuex
My personal neuroscience weblog, you should check it out: The Illuminated Brain - A Weblog on Neuroscience
"It is a capital mistake to theorize before one has data. Insensibly one begins to twist facts to suit theories, instead of theories to suit facts." - Sherlock Holmes
It might be more productive to you start your own thread on this topic
I agree.
My personal neuroscience weblog, you should check it out: The Illuminated Brain - A Weblog on Neuroscience
"It is a capital mistake to theorize before one has data. Insensibly one begins to twist facts to suit theories, instead of theories to suit facts." - Sherlock Holmes
my apologies if i wasn't supposed to post in this thread, i figured that this question wouldn't really need another thread and that i would just bump this one which was related to the discussion. thanks for the info guys
Where's MeD?
I would also be interested if perhaps some of the more knowledgeable posters here had some input on this.
"A mind that is stretched by a new experience can never go back to its' old dimensions"
~Oliver Wendell Holmes, Jr.
A couple more interesting notes. Straight NaCl has an effect, although less potent than the guanine nucleotide, on converting from high to low affinity states. Also cAMP is an activator of Guanine nucleotide exchange factors (GEFs). Forskolin has been shown to increase D2 density and stimulates cAMP. Maybe the connection there is that forskolin changes the apparent D2 density....
Here's what i'm referencing: http://www.ncbi.nlm.nih.gov/pubmed/3157782
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With his girlfriend in England. Nobody knows if he's alive or dead. Reminds me a bit like Schroedinger's cat, lol.
Usually he comes back alive with another insane regimen setup.
My personal neuroscience weblog, you should check it out: The Illuminated Brain - A Weblog on Neuroscience
"It is a capital mistake to theorize before one has data. Insensibly one begins to twist facts to suit theories, instead of theories to suit facts." - Sherlock Holmes
What exactly do you want to know? This is a pretty well-established finding by now.
Can you maybe summarize how downregulation of dopamine receptors works? I used to think that receptors actually disappear after chronic stimulation. But according to that study it seems density is set and only the affinity state of the receptors changes.
Well, you understand this, right?
Agonism = down-regulation (less sensitive to stimulation from agonist, and reduction of receptors on said neuron)
Antagonism = up-regulation (more sensitive to stimulation from agonist, and increase of receptors on said neuron)
Not sure what you're unsure about.
My personal neuroscience weblog, you should check it out: The Illuminated Brain - A Weblog on Neuroscience
"It is a capital mistake to theorize before one has data. Insensibly one begins to twist facts to suit theories, instead of theories to suit facts." - Sherlock Holmes
That was my original understanding. But I must be missing some fundamental concept that caused me to be thrown for a loop by that study.
1. Why does amphetamine, basically an agonist for DA, cause a shift of receptors to high affinity state when antipsychotics also cause a shift to high affinity states?
2. When people use memantine for tolerance, how exactly does upregulation occur? Is there an increase in DA receptors or a kind of state change of existing receptors?
It's still true.
I'm not sure this is known. You have to realize that this process occurs only in some regions on the brain (namely the nigrostriatal system); after all, repeated amphetamine treatment does not cause sensitization to the euphoria! Moreover, the shift of receptors to a high affinity state coincides with normal receptor downregulation. The total number of D2 receptors is decreased, but the remaining receptors have a higher percentage in the D2High state.1. Why does amphetamine, basically an agonist for DA, cause a shift of receptors to high affinity state when antipsychotics also cause a shift to high affinity states?
If I had to guess, I'd suspect the mechanism involves amphetamine's secondary effects. In addition to inducing DA release, amphetamine has glutamatergic properties (though the mechanism seems unclear) and, moreover, amphetamine appears to be an alpha7 nAChR agonist.
Amphetamine induces, through a number of mechanisms, increased NMDA activity in the mesolimbic system. This increase in NMDA activity leads to, among other effects, a decrease in D2 receptor density. Memantine partially blocks this NMDA activation and thus prevents, or attenuates, the reduction in D2 receptor density.2. When people use memantine for tolerance, how exactly does upregulation occur? Is there an increase in DA receptors or a kind of state change of existing receptors?
kassem23 liked this post
WTF, really?
WD with ephedrine is, you're a bit tired for a day, and then back to normal.. IME.
[03:14] FunkOdyssey: dude the only reason nazi's didnt put blacks in concentration camps is because there werent any in germany.
[03:14] FunkOdyssey:if there were they would have put them in before the jews.
[02:15] Sanction no, I whipped out my penis and bludgeoned them
IIRC... there have been some people who when having used ephedrine chronically, and then withdraws, it can induce a certain almost CFS-like state. Maybe this is what ExD is referring to.
My personal neuroscience weblog, you should check it out: The Illuminated Brain - A Weblog on Neuroscience
"It is a capital mistake to theorize before one has data. Insensibly one begins to twist facts to suit theories, instead of theories to suit facts." - Sherlock Holmes
This is why I included "IMO". I don't get withdrawal from amphetamine really, just a return to ADHD symptoms and maybe a subtle hint of anhedonia. But good god, withdrawing from even low doses of ephedrine (12.5mg 3x/day) is a shit for me -- a good week of intense fatigue.
That said, I suspect this all comes down to varying beta adrenergic receptor activity/sensitivity; ephedrine, in addition to being an NE-releaser, is a rather potent beta agonist.
On a related note... when you lower the dose, is it the same thing (just milder) ?
How long should it take to get a reduction in dose fully stable? I know that when you reduce the dose it's a mess for a few days, and I usually go back to my old trusty dose. Maybe I should wait some more.
[quote name='Sonic' timestamp='1300976024' post='654942']I have consumed 5 liters of diet coke per day for the last 6 years and my psychiatrist says that I am perfectly fine with my antipsychotic regime.[/quote]
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