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New member
Anyone know the exact chemcial make up of exticy or have any idea where I can find it?
Whats in Exticy?
- Thread starter JuicedLifter
- Start date
powerhouse7
New member
extacy is a hallucinagen which will make you loose your memory, and other mental problems. You really dont need it.
powerhouse7 said:
Ecstacy is a phenylthylamine - an empathogen. It is not an hallucinogen. Look up Shulgin and Ecstacy and phenylthylamines on Google search engine - see if you can find his book - phenylthylamines I have known and loved.. last time I looked it was there.
Ecstacy is great.. as long as you dont do no more than one a month.
myasshurts
New member
go to bluelight.nu They are more into E than we are into roids.
myasshurts
New member
Pure DXM is white. the color of pills doesn't mean anything but you can get testers that will give you an idea of what is in a pill.
C
Code
Guest
GFI,
Did you spell 'grammar' incorrectly on purpose? *grin*
Kettle, this is pot. Come in Kettle.
Did you spell 'grammar' incorrectly on purpose? *grin*
Kettle, this is pot. Come in Kettle.
VooDoo Lady
New member
GFI said:
Chill out GFI, it was my understanding that this forum was for "off-topic" threads, correct me if I'm wrong.
Additionally, I think that people who live in glass houses shouldn't throw stones. You are admonishing these people for asking about one drug because they are suppose to be asking about another? Humm...seems a BIT hypocritical to me. (and I'm the Queen of all Hypocrites, so I should know one when I see one
)Juiced, if you have specific Q's, I'll try to answer them if I can...PM me if you like.
VDL
Last edited:
yes it does deplete seratonin levels and it depletes them so fast that it destroys the seratonin nerve terminals which causes permanaent brain damage, due to the fact that u cant grow new brain cells.
so doing X only once a month can still lead to adverse effects such as permananent depression, memory loss, and it also makes u dumber because seratonin is needed for higher learning processes.
later
Omar
so doing X only once a month can still lead to adverse effects such as permananent depression, memory loss, and it also makes u dumber because seratonin is needed for higher learning processes.
later
Omar
um....drugs are bad...um
You wanna find out about stuff like GHB, X, LSD or freggin morning glory seeds you should check this resource out. It is all encompassing and based on truth, not what our Gov't shovels to us in 12th grade health class...and every mind altering substance is covered in detail for educated decisions. Peace out.
www.erowid.org
www.erowid.org
You wanna find out about stuff like GHB, X, LSD or freggin morning glory seeds you should check this resource out. It is all encompassing and based on truth, not what our Gov't shovels to us in 12th grade health class...and every mind altering substance is covered in detail for educated decisions. Peace out.
www.erowid.org
www.erowid.org
alexiarenee
New member
You can get a good pill testing kit from
www.eztest.com
only took like 5 days to come on from overseas....
If you get the extreme kind, it breaks all the ingredients in the pill down so you know exactly whats in it...the true x pills are pure MDMA
Just scratch off a tiny piece of the pill and test it.
i dont know if this would be convenient when you are out, and only buy a few to party...but if you are a dealer, its good to make sure YOU are getting good pills to distribute , that way your customers will keep coming back......
www.eztest.com
only took like 5 days to come on from overseas....
If you get the extreme kind, it breaks all the ingredients in the pill down so you know exactly whats in it...the true x pills are pure MDMA
Just scratch off a tiny piece of the pill and test it.
i dont know if this would be convenient when you are out, and only buy a few to party...but if you are a dealer, its good to make sure YOU are getting good pills to distribute , that way your customers will keep coming back......
F
Frackal
Guest
JuicedLifter said:
Don't take this the wrong way, but in my expert opinion, you should avoid brain-cell destroying substances at all costs...
MDMA is primarily a seritonergic (5-HTergic) drug. Serotonin (5-hydroxytrytamine, 5-HT) is one of the major neurotransmitters in the brain, and is synthesized from tryptophan through the intermediate 5-hydroxytryptophan. It is synthesized in 5-HT neurons, and stored in synaptic vesicles. These vesicles release their 5-HT into the synaptic cleft in response to the firing of the 5-HT neurons. In the synaptic cleft the 5-HT neurotransmitter excerts its action on both pre- and post- synaptic receptor sites (sites on the 5-HT neuron itself, and on the neuron which it is communicating with.) 5-HT is then taken back into the 5-HT neuron via the synaptic membrane 5-HT transporter (aka "reuptake pump"), where it is again stored in the synaptic vesicles. 5-HT is metabolized primarily by monoamine oxidase (MAO) into 5-hydroxyindileacetic acid (5-HIAA).
Serotonin is thought to be responsible for many psychological (and physiological) states including mood and sleep. It has been particularly associated with major depression and obsessive compulsive disorder, and drugs to treat these disorders tend to effect 5-HT (although things are not quite clear-cut).
MDMA blocks the reuptake of 5-HT, similarly to SSRI (serotonin specific reuptake inhibiting) anti-depressants such as fluoxetine (Prozac), sertraline, and paroxetine. Unlike those drugs, however, MDMA appears to enter the neuron, either through passive diffusion or directly through the reuptake transporter, and causes the release of 5-HT. This release is calcium-independent (i.e. independent of the firing of the 5-HT neuron) and appears to come from cytoplasmic stores rather than from synaptic vesicles. The released 5-HT then enters the synaptic cleft through the 5-HT transporter. MDMA thus acts on 5-HT similarly to the way amphetamines act on dopamine.
It is thought that this efflux of 5-HT into the synaptic cleft, and the subsequent action of this 5-HT on pre- and post- synaptic binding sites is central to MDMA's neuropharmacology. MDMA, however, has micromolar potency for the serotonin 5-HT2, muscarinic M1, alpha-2 adrenergic and histamine H1 receptors. Agonist (stimulation rather than blocking) properties at the 5-HT2 receptor have been found to fairly universally be associated with "classical" psychedelic drugs such as LSD, psilocybin and mescaline. It is possible that some of MDMA's "psychedelic" effect occurs because of interactions with this receptor. The alpha-2 adrenergic receptor may be associated with some of the carciovascular effects of MDMA. MDMA also releases dopamine which may be central to both its psychological action and to its neurotoxicity in animal studies. Pre- treatment of an animal with a drug which blocks dopamine release will also block MDMA neurotoxicity. Also, serotonin specific releasing agents which are non-dopaminergic have been synthesized and been found to be devoid of MDMA's neurotoxicity in animals, they have also been found to be devoid of MDMA's psychological effects. MDMA tends to indirectly *inhibit* the firing and release of dopamine in nigrostriatal dopamine neurons (neurons projecting from the substantia nigra to the striatum) due to local 5-HT release.
MDMA doses of 20mg/kg in animals can reduce levels of tryptophan hydroxylase, which is the rate-limiting enzyme in 5-HT synthesis. It is thought that this occurs because of oxidative stress which MDMA places on the neuron. This oxidative stress might occur through several possible channels (the metabolism of MDMA into a toxic Quinoid, 5-HT derived toxins, 5-HT mediated cellular events, or temporary inhibition of monoamine oxidase) and the exact mechanism is presently unknown. It is thought that this oxidative stress also leads to the neurodegenerative destruction of 5-HT axons which is observed to occur with large doses of MDMA in animals. Anti-oxidants, anti-dopaminergic agents, agents which block intracellular calcium increases and pre- or post- treatment (up to 6 hours) with fluoxetine all block MDMA's neurotoxicity. Research ontinues on the exact mechanism of MDMA-induced toxicity.
In summary, MDMA effects 5-HT similarly to the way that amphetamines effect dopamine, by inhibiting the reuptake and causing the release of 5-HT. This effect is somewhat similar to the effect that SSRI anti-depressant drugs have. It also effects the 5-HT2 (psychedelic) and alpha-2 adrenergic (cardiovascular) receptor sites. Also, its effects on dopamine appear, at this point, to be involved both with its neurotoxicity and psychological effects.
Serotonin is thought to be responsible for many psychological (and physiological) states including mood and sleep. It has been particularly associated with major depression and obsessive compulsive disorder, and drugs to treat these disorders tend to effect 5-HT (although things are not quite clear-cut).
MDMA blocks the reuptake of 5-HT, similarly to SSRI (serotonin specific reuptake inhibiting) anti-depressants such as fluoxetine (Prozac), sertraline, and paroxetine. Unlike those drugs, however, MDMA appears to enter the neuron, either through passive diffusion or directly through the reuptake transporter, and causes the release of 5-HT. This release is calcium-independent (i.e. independent of the firing of the 5-HT neuron) and appears to come from cytoplasmic stores rather than from synaptic vesicles. The released 5-HT then enters the synaptic cleft through the 5-HT transporter. MDMA thus acts on 5-HT similarly to the way amphetamines act on dopamine.
It is thought that this efflux of 5-HT into the synaptic cleft, and the subsequent action of this 5-HT on pre- and post- synaptic binding sites is central to MDMA's neuropharmacology. MDMA, however, has micromolar potency for the serotonin 5-HT2, muscarinic M1, alpha-2 adrenergic and histamine H1 receptors. Agonist (stimulation rather than blocking) properties at the 5-HT2 receptor have been found to fairly universally be associated with "classical" psychedelic drugs such as LSD, psilocybin and mescaline. It is possible that some of MDMA's "psychedelic" effect occurs because of interactions with this receptor. The alpha-2 adrenergic receptor may be associated with some of the carciovascular effects of MDMA. MDMA also releases dopamine which may be central to both its psychological action and to its neurotoxicity in animal studies. Pre- treatment of an animal with a drug which blocks dopamine release will also block MDMA neurotoxicity. Also, serotonin specific releasing agents which are non-dopaminergic have been synthesized and been found to be devoid of MDMA's neurotoxicity in animals, they have also been found to be devoid of MDMA's psychological effects. MDMA tends to indirectly *inhibit* the firing and release of dopamine in nigrostriatal dopamine neurons (neurons projecting from the substantia nigra to the striatum) due to local 5-HT release.
MDMA doses of 20mg/kg in animals can reduce levels of tryptophan hydroxylase, which is the rate-limiting enzyme in 5-HT synthesis. It is thought that this occurs because of oxidative stress which MDMA places on the neuron. This oxidative stress might occur through several possible channels (the metabolism of MDMA into a toxic Quinoid, 5-HT derived toxins, 5-HT mediated cellular events, or temporary inhibition of monoamine oxidase) and the exact mechanism is presently unknown. It is thought that this oxidative stress also leads to the neurodegenerative destruction of 5-HT axons which is observed to occur with large doses of MDMA in animals. Anti-oxidants, anti-dopaminergic agents, agents which block intracellular calcium increases and pre- or post- treatment (up to 6 hours) with fluoxetine all block MDMA's neurotoxicity. Research ontinues on the exact mechanism of MDMA-induced toxicity.
In summary, MDMA effects 5-HT similarly to the way that amphetamines effect dopamine, by inhibiting the reuptake and causing the release of 5-HT. This effect is somewhat similar to the effect that SSRI anti-depressant drugs have. It also effects the 5-HT2 (psychedelic) and alpha-2 adrenergic (cardiovascular) receptor sites. Also, its effects on dopamine appear, at this point, to be involved both with its neurotoxicity and psychological effects.
buddy28 said:Wodin,
good research. Where did u find ur information? 2 years ago i researched MDMA animal clinical trials. I never uncovered the specificity of dompamine influence on MDMA neurotoxicity. Where did u find dopamine suggested influence on MDMA neurotoxicity?
Cudos
I get a great deal of info from The Vaults of Erowid.
