Dopamine questions...

[Jingleballicks]

I know that dopamine is flooded into your system when you do snow, my question is.. after you come down off the intial euphoria.. what happens? Because it seems I kinda feel down after the intial high, not depressed or anything, but kinda like... I don't really wanna do anything, whats up? Does the dopamine go away? Seems odd

[ganja420]

Hey, I dont know the anwsers to those questions but Ive got a question myself... What is dopamine? Im not into coke so I dont know that much about it.

[white_lighter]

dopamine is that lil chem in your brain that makes you happy

[icemaster]

It's the crash, pretty much all stimulants (coke, E, meth) have this part and yeah it sucks, but its part of drug.

[ganja420]

So white_lighter says its the thing that makes you happy, icemaster sais its the crash and it pretty much sucks.. which one is it? If it makes you happy then it shouldnt suck......... right?

[Micklemouse]

In principle it's both. Dopamine is a
neurotransmitter, as are serotonin and adrenaline(in
fact dopamine is responsible for the production of
adrenaline). Drugs such as cocaine, speed, nicotine,
mdma to an extent, increase the amount of dopamine
released by the brain, whilst at the same time blocking
the brain from reabsorbing it for a time, hence the
high. The crash comes when the block wears off and the
neurotransmitter is rapidly reabsorbed into the brain.
With cocaine and nicotine the amounts of dopamine
released are high, but the blocking action is weak,
explaining why they are so psychologically addicting.
The brain doesn't want the crash, so sends out signals
to delay it - 'Snort another line', 'Smoke another
fag', 'One more rock...', whatever.

Dopamine is involved in the sensations and anticipation
of pleasure, reinforcing the patterns and desires that
keep us eating, having sex and using drugs. It is also
released under stressful and dangerous situations
(remember the adrenaline link - dopamine is needed to
produce adrenaline which is essential to the fight or
flight reflex). It also has a role in controlling our
movements, especially involuntary muscle actions, and
smoothness of movement - depletion and death of
dopamine neurons leads to Parkinson's disease and
similar symptoms (ever wondered why speed and coke
fiends get so twitchy?). It also plays a part in
cognitive function - memory, attention, problem solving
- as well as being linked to psychosis, although the
other neurotransmitters seem to play a part as well
(alter the levels of one and you alter the levels af
the others).

By no means the full picture, but hope it clears things
up a little...

[MacBeth]

I do believe that you are correct when you state that dopamine is responsible for the production of adrenaline, but I have never been able to find out exactly why this is so. I have my own theory about this based on personal experiences and lots of subsequent research on the Internet, but I'm very interested in what you might be able to tell me about this.

[ganja420]

Ahh, I understand now. Thanks a lot.


peace, dan

[Bodhisattva500]

What if someone were to obtain a small amount of pure dopamine Hcl, like 5 ml or something, could this be used as drug, what would happen if ingested?

[rit_guy]

It wouldn't reach your brain, just like serotonin hcl wouldn't. It would affect the receptors in your body though (don't know where they are located), when you ingest serotonin your muscles get really tense for instance.
Of course, you could (in theory) crack a big needle through your skull and hope that you hit the right part of your brain, and inject it.
Yes, a high for 1 second

[chico]

SWIM is a pharmacist and he tells me that while serotonin is responsible for the euphoria/happy/positive effects, dopamine is responsible for the visuals/lights while on Ecstasy. The best ecstasy caps I've ever had are the ones that give great visuals. So I'm under the assumption that these ecstasy pills are dumping more dopamine neurotransmitters and causing themto bindwith my receptors.


Is he right on with his rationale?

[chemicalkid]

Originally Posted by chico

SWIM is a pharmacist and he tells me that while serotonin is responsible for the euphoria/happy/positive effects, dopamine is responsible for the visuals/lights while on Ecstasy. The best ecstasy caps I've ever had are the ones that give great visuals. So I'm under the assumption that these ecstasy pills are dumping more dopamine neurotransmitters and causing themto bindwith my receptors.


Is he right on with his rationale?

I really don't think that is true.

[nanobrain]

^your pharmacisit friend is, um, speaking in grossly generalised terms, and i dont think he is actually correct. non-dopaminergic psychedelics can be incredibly visual.

[Nicaine]

Originally Posted by Micklemouse

The crash comes when the block wears off and the neurotransmitter is rapidly reabsorbed into the brain. With cocaine and nicotine the amounts of dopamine released are high, but the blocking action is weak, explaining why they are so psychologically addicting.

It's even more complicated with nicotine -- the brain has "nicotinic" receptors (actually meant for another chemical called acetylcholine). See these links:

One

Two

Three

Nicotine's a complex drug, affects a number of brain chemicals... one reason among many why IMHO it's the most addictive drug known to man.Edited by: Nicaine

[Zandorf]

i'm oretty sure L-dopa is dopamine that you can orally ingest. i
remember seeing a movie with robin williams and robert deniro, think it
was called awakenings where they administered it to people who
had post-encyphalitic catatonia or something like that, they
were basically paralyzed and the drug woke them up, it was
based on a true story.





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[JewishNazi]

You could try to ingest a large amount of a dopamine precurser in hopes
to get high. Has anyone ever tried methamphetamine with methylphenidate
(ritalin)? Meth promotes the release of dopamine and ritalin stops its
reabsorbtion. In theory, could be quite nice

[boylizard]

Originally Posted by JewishNazi

You could try to ingest a large amount of a dopamine precurser in hopes
to get high. Has anyone ever tried methamphetamine with methylphenidate
(ritalin)? Meth promotes the release of dopamine and ritalin stops its
reabsorbtion. In theory, could be quite nice

no, but swim has found that coke and ritalin go pretty well together. however, the ritalin gives swim a more energetic, tenseness than coke - the coke fixed swims adhd far better than the ritalin -.- unfortunately, even though its scheduled the same, it cant be used. bah.

the coke made swim more alert, more, um.. im not sure how to explain. it completely destroyed my adhd, didnt affect my ocd much, and got rid of my horrible reflexes (plus i dont grab for the right spot when something is thrown at me half the time, it fixed that too)

ritalin does little of this. it just makes me go faster.

[darawk]

@The whole serotonin vs. dopamine visuals side-discussion. The 5-HT2A receptors(which are bound to by almost all classical pyschedelics: lsd, mescalin, psilocin, etc..) inhibit the visual cortex - which is believed to be responsible for most of their hallucinogenic effects. I'd theorize that MDMA's flooding of the brain with real serotonin causes a similar, though less pronounced inhibitive effect on the visual cortex and that is what's responsible for it's visual effects. And AFAIK, no dopamine receptors produce visual alterations, though that may be totally wrong - i've just never heard of dopamine doing anything like that.

[imyourlittlebare]

dopamine does cause visual distortions. meth and cocaine psychosis are possible. Theres the whole dopamine hypothesis of schizophrenia that those patients have too much (experience psychosis and hallucinations) or too little (in a state unable to feel pleasure, ridgid, unresponsive and unmoving). L-dopa can cause these symptoms but also worse ones. there is a non essential amino acid that could help prolong a high. i forget what its called but it possibly prevents the breakdown of endorphins and enkaphalins which in theory could prolong a high for SWIM.

Reputation Comments on this post:

informative

[dmraver]

A little bit more about L-dopa.....
Dopamine, as has been previously discussed, plays an important role in the eurphoric effects of many drugs, specifically amphetamine and cocaine. Dopamine, however, cannot cross the blood brain barrier directly. Thus taking oral dopamine would not help with dopamine deficiencies in the brain very well, but would create significant side effects.

Dopamine is synthesized in the body brain as follows:
(l-phenylalanine -->) l-tyrosine --> l-dopa --> dopamine (---> norepinephrine) (--> --> melanin).
In words, l-tyrosine (an amino acid) is either derived from the diet or produced from l-phenylalanine (another amino acid) in the diet. These can then be converted to levadopa (l-dopa), which crosses the blood/brain barrier and enters the brain. From there is is easily converted to dopamine (DA). One further pathway converts DA to norepinephrine (NE) while another leads to melanin.

Back at the neuron, once the dopamine is released from the post-synaptic terminal, one of the monoamine oxidase enzymes (MAO B I believe) comes through and catabolizes the dopamine, thus removing it from the equation. Long periods of excessive dopaminergic release thus lead to decreased levels of dopamine in the pre-synaptic neurons. The theory is to repalce this dopamine so that transmission across the synapse is not inhibited by dopamine deficiency. Oral L-dopa thus can help in this regard.

Ultimately, however, there is a significant price to for levadopa therapy. A quick google search will certainly demonstrate many of the risks. Additionally, the overstimulation of dopaine synapses outside of the brain these methods would cause or unpleasant to most as well. L-dopa is usually concurrently admnistered with a partial antagonist at DA receptors that fails to cross the blood brain barrier.


While I am not anybody's doctor, the safest way to provide precursors to dopamine might be through l-tyrosine, or indirectly through l-phenylalanine (unless you have PKN). It is possible, however, that excessive consumption of these could have similar reprocussions as L-dopa if used without a similar antagonist. Both of these amino acids are readily available and absorbed from a balanced diet. Hope this helps.

[Nicaine]

Originally Posted by Zandorf

i'm oretty sure L-dopa is dopamine that you can orally ingest.

Oh, what the hell -- Enjoy.

If anyone tries the Mucuna Pruriens, please report your experiences.Edited by: Nicaine

[chico]

Increasing dopamine levels sounds great but doesn't the body/brain still need something to trigger the release of more dopamine from the vesicles, into the synapse, in order to bind with receptors (for yielding the effect that we're all looking for; euphoria)?


I would think that these "Mucuna Pruriens" would be something great to take before dropping E or meth. However, without rolling, your vesicles will just be bloated with x'tra dopamine with no means to release more than the body needs.


Can someone help to clarify this?Edited by: chico

[Nicaine]

Originally Posted by chico

I would think that these "Mucuna Pruriens" would be something great to take before dropping E or meth. However, without rolling, your vesicles will just be bloated with x'tra dopamine with no means to release more than the body needs.


Can someone help to clarify this?

Put it this way, at least one link suggests that L-Dopa can produce euphoria, and Mucuna Pruriens apparently contains L-Dopa. Good enough for me, I'm buyin' me a bottle & trying it.

I know 5-HTP produces many of the effects of boosted serotonin (drowsiness, agitation, anti-depression, etc), I don't see why L-Dopa couldn't do the same for dopamine. I do tend to doubt the effects would be strong enough to solidly qualify as a "high" ... we'll see, tho.Edited by: Nicaine

[chico]

Originally Posted by nanobrain

^your pharmacisit friend is, um, speaking in grossly generalised terms, and i dont think he is actually correct. non-dopaminergic psychedelics can be incredibly visual.

From what I understand, dopamineinduces (biologically)the iris in the eyes while serotonin does notinfluence any iris/eye whatsoever. This would explain how/when dopamine-induced drugs normally always offer nice visuals (things light up/illuminate). Thus, how could serotonin-induced drugs, and thereceptors they triggeroffer visual effects without biologically affecting the eyes in any way?(have you ever heard of someone on Prozac raving about how beautiful things are looking?)


I'm not disputing your claim Nanobrain but from my knowledge it doesn't make sense. Can you tell me what I might be missing here?Edited by: chico

[nanobrain]

^do believe your understandin' may need a helpin, pardner, here's a shamelessly ripped diagram which may be of help:


Figure 1.1. Schematic representation of the pathway from the eye to the pineal gland. SCN- suprachiasmatic nucleus; PVN – paraventricular nucleus; UTC – upper thoracic spinal cord; SCG – superior cervical ganglion; A-R – alpha adrenergic receptor; B-R – beta adrenergic receptor; CREB – cAMP response element binding protein; V – Ventricles of the Brain; C – Capillaries. The arrow behind cAMP indicates an increase in its concentration following stimulation of A-R or B-R by norepinephrine.Edited by: nanobrain

Reputation Comments on this post:

Interesting, informative diagram. Thanks for sharing.