MORE COCAINE SUBSTITUTES!
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james T jame...@mailnet.org
Journal of Clinical Pharmacology. 1987 Apr;27(4):267-70. Bromocriptine therapy in cocaine withdrawal.
Twenty-four cocaine addicts who experienced withdrawal symptoms were studied for six weeks in a double-blind design. Half of the group received daily treatment with bromocriptine and the other half with placebo. Significant relief with bromocriptine was seen almost immediately and continued throughout the detoxification period. The authors speculate that the results are consistent with the "dopamine-depletion model" of cocaine withdrawal.
Journal of Clinical Pharmacology. 1987 Aug;27(8):549-54. Bromocriptine-desipramine protocol in treatment of cocaine addiction.
Thirty-six male cocaine abusers, in withdrawal, were studied for 99 days in a double-blind design. Treatment with bromocriptine was significantly more effective than placebo in alleviating withdrawal symptoms. Adding desipramine to the bromocriptine regimen was significantly more effective than either placebo or bromocriptine alone. The authors hypothesize that these results support a model of dopamine depletion and receptor supersensitivity in cocaine withdrawal.
Psychiatry Res. 1989 Jul;29(1):11-6. Bromocriptine and amantadine in cocaine detoxification.
The effects of bromocriptine and amantadine in treating cocaine withdrawal were compared.
Withdrawal symptoms are thought to be due to central dopamine depletion.
Both bromocriptine and amantadine are dopamine agonists previously reported to diminish withdrawal symptoms.
Thirty subjects were withdrawn for 30 days with amantadine, bromocriptine, or placebo.
Bromocriptine and amantadine were more effective than placebo for 15 days. Amantadine's effectiveness then declined so that it was no more effective than placebo by experiment's end.
Bromocriptine was significantly more effective than both throughout the latter phase of the study.
Amantadine's decline in effectiveness is hypothesized to be due to stimulation of dopamine release.
Neuroscience & Biobehavioural Reviews. 1994 Spring;18(1):121-42.
Pharmacotherapy of cocaine abuse: preclinical development.
Preclinical models of behavioral and toxic effects of cocaine are reviewed and their potential for predicting compounds with efficacy and safety in the medical management of cocaine abuse and toxicity is ***essed. Many of the existing models appear to be good predictors of the effects of compounds against specific behavioral or toxicological actions of cocaine. However, the utility of the models for prediction of the efficacy of new therapeutic entities must await clinical validation as no accepted or standard pharmacotherapy currently exists. Preclinical data generated by these models with drugs currently under clinical investigation for cocaine abuse treatment as well as with other compounds are reviewed. These compounds include buprenorphine, bromocriptine, desmethylimipramine, carbamazepine, dopaminergic agonists, antagonists and partial agonists, dopamine reuptake inhibitors, sigma ligands, serotonin antagonists, and excitatory amino acid antagonists. Preclinical information on several drug cl***es appears sufficiently promising to warrant further evaluation. These include dopamine agonists and partial agonists, D1 receptor antagonists, selective sigma ligands, and modulators of the N-methyl-D-aspartate subtype glutamate receptor.
dur ...@toke.com (Liquid Hat Monster)
interesting, but i just don't like cocaine. it's even more overrated than oxycontin.
-durt
james T jame...@mailnet.org
(My previous post seems to have disappeared) Journal of Clinical Pharmacology. 1987 Apr;27(4):267-70. Bromocriptine therapy in cocaine withdrawal.
Twenty-four cocaine addicts who experienced withdrawal symptoms were studied for six weeks in a double-blind design. Half of the group received daily treatment with bromocriptine and the other half with placebo. Significant relief with bromocriptine was seen almost immediately and continued throughout the detoxification period. The authors speculate that the results are consistent with the "dopamine-depletion model" of cocaine withdrawal.
Journal of Clinical Pharmacology. 1987 Aug;27(8):549-54. Bromocriptine-desipramine protocol in treatment of cocaine addiction.
Thirty-six male cocaine abusers, in withdrawal, were studied for 99 days in a double-blind design. Treatment with bromocriptine was significantly more effective than placebo in alleviating withdrawal symptoms. Adding desipramine to the bromocriptine regimen was significantly more effective than either placebo or bromocriptine alone. The authors hypothesize that these results support a model of dopamine depletion and receptor supersensitivity in cocaine withdrawal.
Psychiatry Res. 1989 Jul;29(1):11-6. Bromocriptine and amantadine in cocaine detoxification.
The effects of bromocriptine and amantadine in treating cocaine withdrawal were compared.
Withdrawal symptoms are thought to be due to central dopamine depletion.
Both bromocriptine and amantadine are dopamine agonists previously reported to diminish withdrawal symptoms.
Thirty subjects were withdrawn for 30 days with amantadine, bromocriptine, or placebo.
Bromocriptine and amantadine were more effective than placebo for 15 days. Amantadine's effectiveness then declined so that it was no more effective than placebo by experiment's end.
Bromocriptine was significantly more effective than both throughout the latter phase of the study.
Amantadine's decline in effectiveness is hypothesized to be due to stimulation of dopamine release.
Neuroscience & Biobehavioural Reviews. 1994 Spring;18(1):121-42.
Pharmacotherapy of cocaine abuse: preclinical development.
Preclinical models of behavioral and toxic effects of cocaine are reviewed and their potential for predicting compounds with efficacy and safety in the medical management of cocaine abuse and toxicity is ***essed. Many of the existing models appear to be good predictors of the effects of compounds against specific behavioral or toxicological actions of cocaine. However, the utility of the models for prediction of the efficacy of new therapeutic entities must await clinical validation as no accepted or standard pharmacotherapy currently exists. Preclinical data generated by these models with drugs currently under clinical investigation for cocaine abuse treatment as well as with other compounds are reviewed. These compounds include buprenorphine, bromocriptine, desmethylimipramine, carbamazepine, dopaminergic agonists, antagonists and partial agonists, dopamine reuptake inhibitors, sigma ligands, serotonin antagonists, and excitatory amino acid antagonists. Preclinical information on several drug cl***es appears sufficiently promising to warrant further evaluation. These include dopamine agonists and partial agonists, D1 receptor antagonists, selective sigma ligands, and modulators of the N-methyl-D-aspartate subtype glutamate receptor.
El Doper Mean Nos...@nospam.au
<snip> First of all: Most of those references are 15 years old. Got any newer ones?
Just because those drugs can help in cocaine withdrawal doesn't mean they act like cocaine. VERY bad ***umption.
princessjess ...@aol.comheresexy (Jessie)
thats what i was thinking... just because it seemed to alleviate cocaine withdrawal somewhat when compared to a placebo, certainly doesn't mean people are going to be out scrambling to get this shit as a alternative to coke!!
jess "Dark clouds may hang on me sometimes, but I'll work it out" Dave Matthews
james T jame...@mailnet.org
Who cares if they're 15 years old? A reference could be 30 years old and still relevant. Let's see what you can come up with, genius.
"Masonic" N...@None.None
I think the point that El Dopey was trying to make is that your 15 year-old references are hardly worthy of posting to a *news* group, are they? I could understand if someone had expressed an interest in the subject matter, but you appear to have spewed forth this information as a result of some kind of literary Tourette syndrome.
Perhaps you would like to explain why you consider this information to be useful to the groups that you crossposted it to (especially for those reading it in alt.drugs.ecstasy).
james T jame...@mailnet.org
Because, dope, a cocaine substitute may also turn out to be an ecstasy substitute!
james T jame...@mailnet.org
I guess you didn't know that most ecstasy substitutes are just stimulants...
msrelentl ...@aol.comthinice (MsRelentless)
In what way is dope a coke substitute? Do you mean that coke is a preferable substance?
To you maybe.
Just wondering what you meant.
Lindsey "If you're walking on thin ice, you may as well dance"
james T jame...@mailnet.org
Psychopharmacology. 1990;100(3):355-60.
Bromocriptine self-administration and bromocriptine-reinstatement of cocaine-trained and heroin-trained lever pressing in rats.
Department of Psychology, Concordia University, Montreal, Canada.
Rats were trained to lever press for intravenous cocaine (1.0 mg/kg/injection) and then switched to bromocriptine (0.3, 1.0, or 3.0 mg/kg/injection) on a FR-1 reinforcement schedule. Bromocriptine sustained responding at all three doses; hourly drug intake increased linearly with log-dose. In a second experiment, animals were trained to respond for cocaine (1.0 mg/kg/injection) or heroin (0.1 mg/kg/injection) reinforcement; drug was available for the first 2 h of each daily session; saline was substituted for cocaine or heroin for 5 subsequent hours.
One hour into each saline substitution session, an intravenous injection of saline or bromocriptine (0.0, 0.5, 1.0, or 2.0 mg/kg) was given. Bromocriptine reinstated both cocaine-trained and heroin-trained lever pressing; under these conditions, the drug was most effective in the heroin-trained animals. Reinforcing doses of clonidine (0.0625 and 0.125 mg/kg), methohexital, and nicotine (0.05 and 0.1 mg/kg), and a sub-intoxicating dose of ethanol (2 g/kg) failed to reinstate cocaine-trained responding. These data indicate that bromocriptine has cocaine-like and heroin-like stimulus and reinforcing effects.
done ...@webtv.net (Michael Donegan)
I think he means "dope" as in "hey you...stupid" not as in "heroin". If I'm right, then this guy sure did pick the wrong way to phrase it, especially on this NG...
Mike
"Masonic" N...@None.None
Cocaine and ecstasy are very different drugs. If, for some strange reason, I were interested finding a substitute for e, I'd be looking for something with the same effects.
"Masonic" N...@None.None
How did you arrive at that conclusion?
travisw ...@hotmail.com (Travisw
Umm congrats at making the most stupid post i've seen awhile. So you think some drug that helps cocaine withdrawal could actually be used as a recreational drug akin to cocaine? Then you go on to say that it could be used as a substitute to MDMA, because if it has recreational cocaine effects then it would also have MDMA effects just based on the fact that MDMA is like cocaine??? Jeezus, I don't want to say you're off-base because that would be a complete understatement
msrelentl ...@aol.comthinice (MsRelentless)
Duhhh to me. I do believe you are right.
Oh well. He did say it wierd.
Thanks.
Lindsey "If you're walking on thin ice, you may as well dance"
BilZ0r Bil...@TAKETHISOUThotmail.com
Well, within the behavioural pharmacology of it, these things are right to a degree. I mean, its about stimulus generalization, training animals to respond in a certain way to a certain drug, i.e. go to the blue room when you're on cocaine, and the red room when you're on placebo. And then giving them a new drug and seeing which room they go to.
Its a preety poor paradigm, and i'm not sure if thats what that guy ment, but it is true in a certain light.
james T jame...@mailnet.org
Because if you read the ****ing labels they all are based on ephedra/caffeine.
james T jame...@mailnet.org
I guess it's just a coincidence that animals will self-administer a dopamine agonist like bromocriptine. (IN fact, animals will self-administer most if not all dopamine agonists) . You're the stupid one who knows nothing about phamacology!
"Masonic" N...@None.None
MDA isn't. MDEA isn't. Various other tryptamines/phenethylamines that give e-like effects aren't. What you are talking about are so-called "herbal highs" - I doubt that many people who have tried ecstasy would fall for these extremely poor alternatives. The only people who consider these a realistic e-substitute are the people that market them.
Don't get me wrong; I'm not trying to say you shouldn't have posted what you posted, but your interpretation of why this information might be useful would have made things a lot clearer.
james T jame...@mailnet.org
I think you'll find that the most common adulterant in street ecstasy is methamphetamine.
teh_lo ...@hotmail.com (Lorax)
I think you'll find that you are wrong, but by your posts I'm guessing you'll never admit it.
james T jame...@mailnet.org
How much do you want to bet? Does anybody have any recent analysis on street ecstasy?
james T jame...@mailnet.org
According to www.ecstasydata.org, caffeine,ephedrine, and methamphetamine (all stimulants) are the 3 most common adulterants of ecstasy.
You obviously have no ****ing clue what you're talking about!
"Masonic" N...@None.None
I expect that it is very common. Adulterants tend to vary from area to area and from time to time. I wasn't really talking about what people take unwittingly when they use "street" ecstasy; more substances with effects similar to e that people deliberately take for that reason.
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