89 replies to this topic

[truboy]

 

 

My subjective experience with forskolin is that it does make me more sensitive to the highs of life.  Smoking a cigarette can give me a really powerful rush and my libido seems stronger.  On other forums people claim it helps against amphetamine tolerance.

 

Keep up the good work, OP.

Here is my experience(be free to call it anicdote)

Forskolin made me better in relating to others. Made conversations more enjoyable.

But at the same time seems made me stupid.

 

 

What do you define as 'stupid' in this case? I'm curious about your criteria, because there may be an easy explanation for that, or at least, the perception of it.
 

 

 

Don't remember exactly what i felt/what made me come to that conclusion. But i remeber that i made dicision to stop it and 'make me stupid' was exactly the my reasoning/explanation. Though there were some pluses - 'relating to others' better one of them.

[HappyShoe]

Nice new avi HS.

 

 

 

Thanks =)               Figured it was about time I got one. I was originally going to have my friend take a picture of her shoes, of which I was supposed to be one, but apparently they have been lost or ruined. Hurray for google! lol

[HappyShoe]

 

 

 

My subjective experience with forskolin is that it does make me more sensitive to the highs of life.  Smoking a cigarette can give me a really powerful rush and my libido seems stronger.  On other forums people claim it helps against amphetamine tolerance.

 

Keep up the good work, OP.

Here is my experience(be free to call it anicdote)

Forskolin made me better in relating to others. Made conversations more enjoyable.

But at the same time seems made me stupid.

 

 

What do you define as 'stupid' in this case? I'm curious about your criteria, because there may be an easy explanation for that, or at least, the perception of it.
 

 

 

Don't remember exactly what i felt/what made me come to that conclusion. But i remeber that i made dicision to stop it and 'make me stupid' was exactly the my reasoning/explanation. Though there were some pluses - 'relating to others' better one of them.

 

The reason I say this, is because an increase in dopamine can cause an increase in the number and flow rate of thoughts you have, and it is very likely for someone to have a thought they condemn, or associate with a negative scenario in a social setting at the time, and think they are 'stupid' because of it. I myself have a lot of intrusive thoughts/negative memories of moments where I said something stupid or such, and I call myself 'stupid' reflexively before I have a chance to reassure myself that isn't the case.
Another possibility is, that people's level of self discipline and metacognitive structure isn't on the same level as their ability to think and process information, and thereby their thoughts are somewhat chaotic and disorganized with such an increase in mental energy that they aren't used to, can lead to mistakes one could call 'stupid'. A good example of this, is a well behaved child drinking a bunch of soda, or coffee, and becoming 'hyper' and reckless, annoying, etc.

I remember when I was prescribed amphetamines, I thought so quickly, and had such complex thoughts, that it was difficult to keep track of all of it, so I tended to be a little 'ranty' in conversations. It often involved sharing every thought I had on things from multiple perspectives, rather than only those thoughts I would have chosen or agreed with personally.

Not saying this was the case with you, but it might be worth considering here.

[Arjuna]

Raised cAMP (which forskolin causes) is known to impair the prefrontal cortex, which may or may not be the cause of what you experienced. The prefrontal cortex is kind of the organizer for the brain.

Edited by Arjuna, 14 February 2015 - 07:45 AM.

[normalizing]

 

area1255 caused this flamewar. he is a troublemaker!

That's not what the moderators said, looks like you're not doing so well in the objective oriented department?

Good Luck,

 

 

hah i said you caused the flamewar and here you go, supporting my statement, thanks

[Area-1255]

 

 

area1255 caused this flamewar. he is a troublemaker!

That's not what the moderators said, looks like you're not doing so well in the objective oriented department?

Good Luck,

 

 

hah i said you caused the flamewar and here you go, supporting my statement, thanks

 

I proved you are a troll and you have a major inferiority complex, especially since you * actually started this flame war. 

 

 

 

cocaine is still the only and best dopamine booster i have had and i tried around 50 pills and herbs so i know. im just trying to figure out if its just the dopamine tho, maybe cocaine affects the NMDA system in some way? i cant find reliable info on this, but anyone has a clue, barbelith??

 

 

 

@Area-1255:
I am not saying that any of this is is wrong, but do you really believe that your words will gain more power if you make them look like you are screaming and use other means of non-standard emphasis that seek to annoy the way in which other people perceive the world?

My words have "power"  either way  - and plenty of people like the way I write....

It signifies definitions, not loops.  

 

 

your words are siezure inducers. and plenty of people DONT like them.

it signifies annoyance, not "definitions"

 

 

Edited by Area-1255, 14 February 2015 - 11:51 AM.

[Area-1255]

. 

 

Edited by Area-1255, 14 February 2015 - 11:50 AM.

[Flex]

 

cocaine is still the only and best dopamine booster i have had and i tried around 50 pills and herbs so i know. im just trying to figure out if its just the dopamine tho, maybe cocaine affects the NMDA system in some way? i cant find reliable info on this, but anyone has a clue, barbelith??

Cocaine activates multiple pathways, it's a triple reuptake inhibitor - therefore it enhances norepinephrine and serotonin as well.

Norepinephrine is known to modulate dopamine and give a great energy burst in small-moderate amounts, it also contributes to "sensory euphoria".

 

 

It has been show to be a inverse inhibitor at DAT, thus reversing the dopamine flow and increasing therefore the dopamine concetration.

Methylphenidate has been assumed to work like thisas well, because e.g. buprenorphine, a DRI, isnt able to cause euphoria as well as some test substitutes for cocaine addiction, albeit beeing far more potent DRI inhibitors.
 

Edited by Flex, 14 February 2015 - 06:41 PM.

[the_apollo]

So can we get back on track with the topic?

 

What increases dopamine D2 receptor level in the brains reward center (NAcc) and also in the rest of the striatum,, ?

 

 

[HappyShoe]

Well, you already mentioned inositol and a few other things.
Citicoline and sulbutiamine increase d2 receptors, although off the top of my head I'm not sure if it's specifically in reward centers.

[Area-1255]

Well, you already mentioned inositol and a few other things.
Citicoline and sulbutiamine increase d2 receptors, although off the top of my head I'm not sure if it's specifically in reward centers.

Inositol does, it's active in the striatum especially.

http://www.ncbi.nlm.nih.gov/pubmed/11267629

 

Pharmacol Biochem Behav. 2001 Feb;68(2):245-53.

Chronic inositol increases striatal D(2) receptors but does not modify dexamphetamine-induced motor behavior. Relevance to obsessive-compulsive disorder.

Harvey BH1, Scheepers A, Brand L, Stein DJ.

Author information

• 1Department of Pharmacology, School of Pharmacy, Potchefstroom University for Christian Higher Education, 2520, Potchefstroom, South Africa. fklbhh@puknet.puk.ac.za

Abstract

A large body of evidence suggests that the neuropathology of obsessive-compulsive disorder (OCD) lies in the complex neurotransmitter network of the cortico-striatal-thalamo-cortical (CSTC) circuit, where dopamine (DA), serotonin (5HT), glutamate (Glu), and gamma-amino butyric acid (GABA) dysfunction have been implicated in the disorder. Chronic inositol has been found to be effective in specific disorders that respond to selective serotonin reuptake inhibitors (SSRIs), including OCD, panic, and depression. This selective mechanism of action is obscure. Since nigro-striatal DA tracts are subject to 5HT(2) heteroreceptor regulation, one possible mechanism of inositol in OCD may involve its effects on inositol-dependent receptors, especially the 5HT(2) receptor, and a resulting effect on DA pathways in the striatum. In order to investigate this possible interaction, we exposed guinea pigs to oral inositol (1.2 g/kg) for 12 weeks. Subsequently, effects on locomotor behavior (LB) and stereotype behavior (SB), together with possible changes to striatal 5HT(2) and D(2) receptor function, were determined. In addition, the effects of chronic inositol on dexamphetamine (DEX)-induced motor behavior were evaluated. Acute DEX (3 mg/kg, ip) induced a significant increase in both SB and LB, while chronic inositol alone did not modify LA or SB. The behavioral response to DEX was also not modified by chronic inositol pretreatment. However, chronic inositol induced a significant increase in striatal D(2) receptor density (B(max)) with a slight, albeit insignificant, increase in 5HT(2) receptor density. This suggests that D(2) receptor upregulation may play an important role in the behavioral effects of inositol although the role of the 5HT(2) receptor in this response is questionable.

PMID:   11267629   [PubMed - indexed for MEDLINE]

[HappyShoe]

I'm getting really sick of these trolls down-voting for no reason.

 

[Area-1255]

I'm getting really sick of these trolls down-voting for no reason.

And it's literally non-selective, like a dragon spewing fire on an entire city instead of just one village. Must reflect their unstable personalities.

[HappyShoe]

http://www.reddit.co...und_effects_on/

What do you guys think of this. Seems it's yadayada's post on reddit.
I was looking into upregulating Tyrosine Hydroxylase as a way of increasing dopamine.
Seems Bromantane(Ladasten) does this?

I'm curious if this would be permanent/long lasting, and how long would it take to achieve this effect.
Would it have an opposite effect after too long?
 

[Area-1255]

http://www.reddit.co...und_effects_on/

What do you guys think of this. Seems it's yadayada's post on reddit.
I was looking into upregulating Tyrosine Hydroxylase as a way of increasing dopamine.
Seems Bromantane(Ladasten) does this?

I'm curious if this would be permanent/long lasting, and how long would it take to achieve this effect.
Would it have an opposite effect after too long?
 

I doubt if tyrosine hydroxylase would downregulate, it's an enzyme not a receptor or G-protein related substance; which have far more sophistication but also a better capacity for homeostatic interexchangeability.

Being bromantane became listed as a "doping agent" - and given it's track record by athletes and in extensive lab testing,  I would suspect long-term use is actually quite reliable!

Edited by Area-1255, 18 February 2015 - 01:56 AM.

[HappyShoe]

I completely forgot they sell it at tht.co! Stumbled upon a coupon code "ALCHEMY10" from metabolicalchemy.
There is some nifty info about it increasing the strength of the immune system too.

What a novel way to increase dopamine levels!

Sad thing is, I bought some of this a while ago, and I took it once, and then forgot about it forever, and then threw it away because I considered it worthless.
Pretty sure I thought it was making me nauseous too, although at the time I was experimenting with weird herbs and such, so bad call on my part. =P

[normalizing]

 

 

 

area1255 caused this flamewar. he is a troublemaker!

That's not what the moderators said, looks like you're not doing so well in the objective oriented department?

Good Luck,

 

 

hah i said you caused the flamewar and here you go, supporting my statement, thanks

 

I proved you are a troll and you have a major inferiority complex, especially since you * actually started this flame war. 

 

 

 

cocaine is still the only and best dopamine booster i have had and i tried around 50 pills and herbs so i know. im just trying to figure out if its just the dopamine tho, maybe cocaine affects the NMDA system in some way? i cant find reliable info on this, but anyone has a clue, barbelith??

 

 

 

@Area-1255:
I am not saying that any of this is is wrong, but do you really believe that your words will gain more power if you make them look like you are screaming and use other means of non-standard emphasis that seek to annoy the way in which other people perceive the world?

My words have "power"  either way  - and plenty of people like the way I write....

It signifies definitions, not loops.  

 

 

your words are siezure inducers. and plenty of people DONT like them.

it signifies annoyance, not "definition

 

 

 

 

you are the one with major inferiority complex here, keep replying to me trying to somehow influence, change my mind in sick twisted way with your pseudoscience references and statement. im sick of your weakness being so exposed ktnx.

[Area-1255]

 

 

 

 

area1255 caused this flamewar. he is a troublemaker!

That's not what the moderators said, looks like you're not doing so well in the objective oriented department?

Good Luck,

 

 

hah i said you caused the flamewar and here you go, supporting my statement, thanks

 

I proved you are a troll and you have a major inferiority complex, especially since you * actually started this flame war. 

 

 

 

cocaine is still the only and best dopamine booster i have had and i tried around 50 pills and herbs so i know. im just trying to figure out if its just the dopamine tho, maybe cocaine affects the NMDA system in some way? i cant find reliable info on this, but anyone has a clue, barbelith??

 

 

 

@Area-1255:
I am not saying that any of this is is wrong, but do you really believe that your words will gain more power if you make them look like you are screaming and use other means of non-standard emphasis that seek to annoy the way in which other people perceive the world?

My words have "power"  either way  - and plenty of people like the way I write....

It signifies definitions, not loops.  

 

 

your words are siezure inducers. and plenty of people DONT like them.

it signifies annoyance, not "definition

 

 

 

 

you are the one with major inferiority complex here, keep replying to me trying to somehow influence, change my mind in sick twisted way with your pseudoscience references and statement. im sick of your weakness being so exposed ktnx.

 

So you admitted I changed your mind? The first step to admitting your defeat is acknowledging that I'm inside your head - I control you fool! 

[HappyShoe]

Normalizing. Seriously!? We were back on topic and you dredge up this crap again out of nowhere!
Stop.

Stahp.

Stop.

Good?
No more of this.

[Area-1255]

Normalizing. Seriously!? We were back on topic and you dredge up this crap again out of nowhere!
Stop.

Stahp.

Stop.

Good?
No more of this.

Normalizing is an instigative troll who loves attention...poor kid.

[FunkOdyssey]

It takes two people to make a thread devolve into a flame war.  As soon as one of you is mature enough to disengage, it's over.  Will the bigger man please step forward and STFU?

[truboy]

Guys can you explain what Dopamine D2/3 Receptors mean?

I know there are D2 receptors, D3 receptors (besides D1, D4, D5)

And this D2/3 mean what? 'D2 and D3'. Or 'ratio of D2 to D3'.

[Area-1255]

Guys can you explain what Dopamine D2/3 Receptors mean?

I know there are D2 receptors, D3 receptors (besides D1, D4, D5)

And this D2/3 mean what? 'D2 and D3'. Or 'ratio of D2 to D3'.

If you go through the thread and read a little more carefully, you would understand. 

Look at the context of what is written.

D2/D3 is referring them both in the same sentence, because there are comparable / similar effects between both receptors, and they are both considered "D2-Like" receptors...given their similarity in biological function*.

 

D1 receptors and D5 are both considered D1-like dopamine receptors, because D5 was cloned shortly after and considered like , in structure and function the D1 receptor....both of these receptors are positively coupled to G-proteins and both activate adenylate cyclase which leads to increased  cAMP - which then leads to some degree of stimulation and calcium channel activation.

 

D2-D3-D4 are all D2-like receptors, they all are negatively coupled to G-proteins with similar biological effects but with distribution that densitites that vary and thus effect researchable outcomes.

D2 receptors have autoreceptors which function to decrease dopamine synthesis / neuron activity...two distinct pathways, but the autoreceptors are ONLY the pre-synaptic ones (D2s), whereas D2 L = D-2-"Long" has it's post-synaptic effects and a stronger downstream effect more indicative of a dopaminergic pathway and having more interaction with the D1-like receptors...

 

 

D1 and D5 are largely involved in behavioral responses and energy production/expenditure, they both play a role in cocaine induced hyper-excitation and euphoria, and are necessary in the study of anxiety disorders and depression. 

 

D2,D3,D4 have some similar effects; are involved in memory, sexuality, depressive-phases, response to light and affect heart rate via a central mechanisms - they have involvement in addiction as well and tend to play a role in "channeling" neural activity leading to more transient states if excessively activated....

 

As I've said, the main reason why dopamine drugs have side-effects is because they activate only D2-like, if they activated both families there would be far less side-effects altogether...

 

The body/mind is not really set up or made to just accept dopaminergic inputs to one family-type, therefore dopamine drugs are seen as very strange to the human body and it only gets balanced out when you find a separate way to re-activate the cyclic adensoine monophosphate symptoms (as would be done by activating D1-D5 complex's)..therefore, I don't recommend dopamine drugs without the use of either forskolin, or more preferably, a histamine H3 antagonist such as conessine or pitolisant.

[BieraK]

 

http://www.reddit.co...und_effects_on/

What do you guys think of this. Seems it's yadayada's post on reddit.
I was looking into upregulating Tyrosine Hydroxylase as a way of increasing dopamine.
Seems Bromantane(Ladasten) does this?

I'm curious if this would be permanent/long lasting, and how long would it take to achieve this effect.
Would it have an opposite effect after too long?
 

I doubt if tyrosine hydroxylase would downregulate, it's an enzyme not a receptor or G-protein related substance; which have far more sophistication but also a better capacity for homeostatic interexchangeability.

Being bromantane became listed as a "doping agent" - and given it's track record by athletes and in extensive lab testing,  I would suspect long-term use is actually quite reliable!

 

After taking selegiline for six months I developed tolerance to it, after doing a little research I found this:
http://www.ncbi.nlm..../pubmed/1350320
however this other study says the contrary
http://www.ncbi.nlm..../pubmed/9191076

Apparently my experience is more related to the first study.

Concerning to bromantane, after reading user experiences I think that 9 mebc is better for a classical "dopaminergic" effect, bromantane has a more anti-anxiety calming with focus effect. 

Perhaps Selegiline+Lithium orotate could be a good combination, lithium regulates mood and increase Tyrosine Hydroxylase expression.

[truboy]

 

Guys can you explain what Dopamine D2/3 Receptors mean?

I know there are D2 receptors, D3 receptors (besides D1, D4, D5)

And this D2/3 mean what? 'D2 and D3'. Or 'ratio of D2 to D3'.

If you go through the thread and read a little more carefully, you would understand. 

Look at the context of what is written.

D2/D3 is referring them both in the same sentence, because there are comparable / similar effects between both receptors, and they are both considered "D2-Like" receptors...given their similarity in biological function*.

 

D1 receptors and D5 are both considered D1-like dopamine receptors, because D5 was cloned shortly after and considered like , in structure and function the D1 receptor....both of these receptors are positively coupled to G-proteins and both activate adenylate cyclase which leads to increased  cAMP - which then leads to some degree of stimulation and calcium channel activation.

 

D2-D3-D4 are all D2-like receptors, they all are negatively coupled to G-proteins with similar biological effects but with distribution that densitites that vary and thus effect researchable outcomes.

D2 receptors have autoreceptors which function to decrease dopamine synthesis / neuron activity...two distinct pathways, but the autoreceptors are ONLY the pre-synaptic ones (D2s), whereas D2 L = D-2-"Long" has it's post-synaptic effects and a stronger downstream effect more indicative of a dopaminergic pathway and having more interaction with the D1-like receptors...

 

 

D1 and D5 are largely involved in behavioral responses and energy production/expenditure, they both play a role in cocaine induced hyper-excitation and euphoria, and are necessary in the study of anxiety disorders and depression. 

 

D2,D3,D4 have some similar effects; are involved in memory, sexuality, depressive-phases, response to light and affect heart rate via a central mechanisms - they have involvement in addiction as well and tend to play a role in "channeling" neural activity leading to more transient states if excessively activated....

 

As I've said, the main reason why dopamine drugs have side-effects is because they activate only D2-like, if they activated both families there would be far less side-effects altogether...

 

The body/mind is not really set up or made to just accept dopaminergic inputs to one family-type, therefore dopamine drugs are seen as very strange to the human body and it only gets balanced out when you find a separate way to re-activate the cyclic adensoine monophosphate symptoms (as would be done by activating D1-D5 complex's)..therefore, I don't recommend dopamine drugs without the use of either forskolin, or more preferably, a histamine H3 antagonist such as conessine or pitolisant.

 

 

WOW. Simply WOW. Very researched and knowledgeable answer. I was missing a lot in understanding of D receptors.
Could you point me in the natural ways to upregulate D2 receptors in striatum?

Besides CDP-choline, inisitol, forskolin and exersizes? A there any other natural ways.?

[Area-1255]

 

 

Guys can you explain what Dopamine D2/3 Receptors mean?

I know there are D2 receptors, D3 receptors (besides D1, D4, D5)

And this D2/3 mean what? 'D2 and D3'. Or 'ratio of D2 to D3'.

If you go through the thread and read a little more carefully, you would understand. 

Look at the context of what is written.

D2/D3 is referring them both in the same sentence, because there are comparable / similar effects between both receptors, and they are both considered "D2-Like" receptors...given their similarity in biological function*.

 

D1 receptors and D5 are both considered D1-like dopamine receptors, because D5 was cloned shortly after and considered like , in structure and function the D1 receptor....both of these receptors are positively coupled to G-proteins and both activate adenylate cyclase which leads to increased  cAMP - which then leads to some degree of stimulation and calcium channel activation.

 

D2-D3-D4 are all D2-like receptors, they all are negatively coupled to G-proteins with similar biological effects but with distribution that densitites that vary and thus effect researchable outcomes.

D2 receptors have autoreceptors which function to decrease dopamine synthesis / neuron activity...two distinct pathways, but the autoreceptors are ONLY the pre-synaptic ones (D2s), whereas D2 L = D-2-"Long" has it's post-synaptic effects and a stronger downstream effect more indicative of a dopaminergic pathway and having more interaction with the D1-like receptors...

 

 

D1 and D5 are largely involved in behavioral responses and energy production/expenditure, they both play a role in cocaine induced hyper-excitation and euphoria, and are necessary in the study of anxiety disorders and depression. 

 

D2,D3,D4 have some similar effects; are involved in memory, sexuality, depressive-phases, response to light and affect heart rate via a central mechanisms - they have involvement in addiction as well and tend to play a role in "channeling" neural activity leading to more transient states if excessively activated....

 

As I've said, the main reason why dopamine drugs have side-effects is because they activate only D2-like, if they activated both families there would be far less side-effects altogether...

 

The body/mind is not really set up or made to just accept dopaminergic inputs to one family-type, therefore dopamine drugs are seen as very strange to the human body and it only gets balanced out when you find a separate way to re-activate the cyclic adensoine monophosphate symptoms (as would be done by activating D1-D5 complex's)..therefore, I don't recommend dopamine drugs without the use of either forskolin, or more preferably, a histamine H3 antagonist such as conessine or pitolisant.

 

 

WOW. Simply WOW. Very researched and knowledgeable answer. I was missing a lot in understanding of D receptors.
Could you point me in the natural ways to upregulate D2 receptors in striatum?

Besides CDP-choline, inisitol, forskolin and exersizes? A there any other natural ways.?

 

No, not that I can think of right now, quite honestly, regulating or increasing receptor expression is something done more easily with pharmaceuticals; tianeptine and phenyl piracetam together with inositol / CDP-Choline should result in a 7-fold increase in dopamine D2 receptor concentration abroad.

[HappyShoe]

Is there a way to upregulate D1/D5 receptors?
I would think this would be relevant to those of us who have had negative experiences with such medications?
It seems that NMDA activation does this according to this ( http://www.jneurosci...5/1149.full.pdf )
At first I was thinking that this might explain why Memantine helps to reverse amphetamine tolerance, but it seems that it's not NMDA antagonists which control this mechanism, but agonism or perhaps positive allosteric modulation? Is there even such a thing as that for glutamate?

 

Guys can you explain what Dopamine D2/3 Receptors mean?

I know there are D2 receptors, D3 receptors (besides D1, D4, D5)

And this D2/3 mean what? 'D2 and D3'. Or 'ratio of D2 to D3'.

If you go through the thread and read a little more carefully, you would understand. 

Look at the context of what is written.

D2/D3 is referring them both in the same sentence, because there are comparable / similar effects between both receptors, and they are both considered "D2-Like" receptors...given their similarity in biological function*.

 

D1 receptors and D5 are both considered D1-like dopamine receptors, because D5 was cloned shortly after and considered like , in structure and function the D1 receptor....both of these receptors are positively coupled to G-proteins and both activate adenylate cyclase which leads to increased  cAMP - which then leads to some degree of stimulation and calcium channel activation.

 

D2-D3-D4 are all D2-like receptors, they all are negatively coupled to G-proteins with similar biological effects but with distribution that densitites that vary and thus effect researchable outcomes.

D2 receptors have autoreceptors which function to decrease dopamine synthesis / neuron activity...two distinct pathways, but the autoreceptors are ONLY the pre-synaptic ones (D2s), whereas D2 L = D-2-"Long" has it's post-synaptic effects and a stronger downstream effect more indicative of a dopaminergic pathway and having more interaction with the D1-like receptors...

 

 

D1 and D5 are largely involved in behavioral responses and energy production/expenditure, they both play a role in cocaine induced hyper-excitation and euphoria, and are necessary in the study of anxiety disorders and depression. 

 

D2,D3,D4 have some similar effects; are involved in memory, sexuality, depressive-phases, response to light and affect heart rate via a central mechanisms - they have involvement in addiction as well and tend to play a role in "channeling" neural activity leading to more transient states if excessively activated....

 

As I've said, the main reason why dopamine drugs have side-effects is because they activate only D2-like, if they activated both families there would be far less side-effects altogether...

 

The body/mind is not really set up or made to just accept dopaminergic inputs to one family-type, therefore dopamine drugs are seen as very strange to the human body and it only gets balanced out when you find a separate way to re-activate the cyclic adensoine monophosphate symptoms (as would be done by activating D1-D5 complex's)..therefore, I don't recommend dopamine drugs without the use of either forskolin, or more preferably, a histamine H3 antagonist such as conessine or pitolisant.

 

 

Edited by HappyShoe, 03 March 2015 - 10:23 PM.

[Area-1255]

 

Is there a way to upregulate D1/D5 receptors?
I would think this would be relevant to those of us who have had negative experiences with such medications?
It seems that NMDA activation does this according to this ( http://www.jneurosci...5/1149.full.pdf )
At first I was thinking that this might explain why Memantine helps to reverse amphetamine tolerance, but it seems that it's not NMDA antagonists which control this mechanism, but agonism or perhaps positive allosteric modulation? Is there even such a thing as that for glutamate?

 

Pregnenolone, DHEA, increase DHT levels and use of Piracetam will upregulate NMDA receptors, doing a simple search in google "how to upregulate NMDA receptors" yields my articles / submissions quickly 

Additionally, antagonizing histamine H3 receptors with pitolisant, betahistine or connessine will help improve D1 function and NMDA function.

http://www.bluelight...-NMDA-receptors

http://www.shroomery...Number/19016758

http://www.longecity...pregulate-nmda/

http://area1255.blog...eptors-and.html

[HappyShoe]

Cool thanks for the response. Seems like my exercise regimen will help with the DHEA and histamine, I'll take Pregnenolone sublingual tincture and I'll use Coluracetam with Pitolisant. =)

[truboy]

Seems like Amantadine increases striatal d2 receptor density:

Amantadine, is a non competitive NMDA receptors antagonist that has been proved beneficial in Parkinson's disease. However its mechanism of action at therapeutic doses is still under discussion. Aim of this study was to evaluate the effect of repeated administration of amantadine on striatal dopaminergic system by measuring [11C]raclopride binding to striatal D2 dopamine receptors, in patients with moderate idiopathic Parkinson's disease. Eight patients completed the study undergoing a PET scan, before and after 10–14 days treatment with Amantadine (200 mg/day). Patients were on treatment with L-DOPA, which was suspended 1 night before each PET scans, and free from dopaminergic agonists, anticholinergic and antidepressants. Amantadine treatment significantly increased [11C-]Raclopride binding (caudate: 10% p = 0.04; putamen 11% p = 0.01). A slight reduction (−7.3%, p = 0.062) of UPDRS total scores was also observed. The increased availability of striatal D2 receptors, is likely to be caused by drug induced modification of receptors expression. This hypothesis is consistent with previous experiments, indicating an increase in striatal D2 receptors in rats treated with amantadine or other non competitive NMDA antagonists and suggests that the neo-synthesis of D2 receptors may represent a reinforcing mechanism of drug efficacy.