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Question about drugs.....
- Thread starter myway
- Start date
S
Spartacus
Guest
keep tryin`
needtogetaas
New member
wtf.
I don't know him but where is that JH1 dood or whatever his name was?
S
Spartacus
Guest
my fantasy sandwich of me,myway and ms willow gets better and better
I need to do some preparatory cardio
I need to do some preparatory cardio
all the whey
New member
The probably have Adhd.
My friend was like that. I met him when I entered the big house. He doesnt feel shit. He's a frickin mummy.
all the whey
New member
what nimbus said
needtogetaas
New member
I tried coke once. I sniffed about 3 lines and felt nothing at all. I have adhd. Is this true? Every one elce was getting high and I was like wtf is so great about this shit. It sucks I am not getting a thing.all the whey said:
S
Spartacus
Guest
hehCal_21 said:
all the whey
New member
needtogetaas said:
I have adhd. But, I never tried coke. However, I have heard a lot of others with it get little reaction from coke.
Fuck Yo Couch!!!!!!
S
Spartacus
Guest
male fraudsuperdave said:
superdave said:
Underground cage fighting....in Beirut.
needtogetaas
New member
Now I sniffed a huge pile of ridalin once and got fucked up lol.all the whey said:
needtogetaas said:
Adhd = Attention-Deficit Hyperactivity Disorder?
needtogetaas
New member
yes and I have add to.the_alcatraz said:
needtogetaas
New member
LOL wtf ever.myway said:
needtogetaas said:
My doctor says I have partial ADHD.
S
Spartacus
Guest
how do I fake a test for adhd?
I`m getting tested april 14th
I want adderal
I`m getting tested april 14th
I want adderal
Spartacus said:
act like you can't concentrate on shit...like you dnt have enough analytical skillz and like you can do smthg for so long, then you need to change into doing something else.
Coke never did shit for me. Just make nasty shit run down the back of my throat and numb whatever it touches. Complete waste!
S
Spartacus
Guest
this is what I plan to dojavaguru said:Look up the symptoms and mimic them...you can google it. If the 1st Doc doesn't give it to you then find another that will.
this doc is my third attempt
and she`s got me to take th test
so far then it`s a go
this is what I want for an anti-depressant
it`s probably the best for depression
but doctors are skittish to prescibe because of the abuse potential
because the damn rats in the tests keep pulling the lever to self administer
well no shit
it works
it`s frustrating because I`ve been through around a dozn anti-depressants and they all have bad sides,esp. sexual retardation
I take wellbutrin,but it only partially works
amphetamine works
I don`t even want to take it daily
just on down days
One of the strippers I use to date is asking me for adderal, said something about dieting. wtf is that stuff?
all the whey
New member
PuddleMonkey said:
It is a stim that will kill appetite.
A lot of Strippers do use them.lol
all the whey said:
Weird, I use to get them all ephedra for the longest time but then started keeping it all for me once supply got slim.
S
Spartacus
Guest
that`s fairly accurate too.I`ve changed from say a decade ago. I used to play highly complex military strategy games..some requiring around 3 hours of caculations and ploting before you advanced to the next turnthe_alcatraz said:
hours and hours a night
pissed the wife off
now I constantly shift fom posting on the net..reading a magazine or paper for a few..and then watching TV...back and forth and back and forth
Spartacus said:
decreased concentration is usually a first symptom of ADHD.
javaguru said:
Pretty much yeah.
S
Spartacus
Guest
what?
she`s Jewish
the doc
she`s Jewish
the doc
javaguru said:The only advice I can give is to give the party line.
For example, just call all the Nazi camps "death camps" and don't try to explain the difference between a work camp and a "death camp."
olololoololololololo
S
Spartacus
Guest
yesterday I cremated the daughter of a pair of concentration camp survivorsjavaguru said:The only advice I can give is to give the party line.
For example, just call all the Nazi camps "death camps" and don't try to explain the difference between a work camp and a "death camp."
the minister just told me that when I noticed she was from Germany
the irony
all the whey
New member
cindylou said:
Pud can hook you and your sis up.
Just tell him what club you dance at.
all the whey said:
lol bastard!
LOL...nice lookin gangbanger...lmao
S
Spartacus
Guest
for adderal i wouldn't mind paying out of pocketcindylou said:
I got a scrip for meridia once
$160 for 30 and insurance didn't cover it
that hurt
ceo said:That's Rick James, bitch!!
ololololololololo
txbondsman
New member
all the whey said:
<<< add w/o the h, it takes more to feel the same way as others, with just a few lines or so, it'll usually make you sleepy or very relaxed. If you keep doing it, way past when your friends are bouncing off the walls, you will eventually get there. I've never seen someone who could never get a buzz no matter how much they took....
myway said:
He might be a terminator.
hanselthecaretaker said:
olololololololololo
S
Spartacus
Guest
take the drugs and hide them at the same timePICK3 said:
Spartacus said:
Only if you're in prison.
needtogetarmy
CEO of Project Mayhem
I know a few people who cannot get high on coke. It is a receptor issue in the brain.
I read a while back they found something related to cocaine (and nicotine) and they are working on a vaccine that will inhibit its uptake to the brain.
Imagine being immunized to cocaine or nicotine. It would solve a lot of social issues.
I've never use the stuff, no weed or anything else. Alcohol kicked my ass once or twice. I could just imagine what cocaine would do. I would be a junkie.
I read a while back they found something related to cocaine (and nicotine) and they are working on a vaccine that will inhibit its uptake to the brain.
Imagine being immunized to cocaine or nicotine. It would solve a lot of social issues.
I've never use the stuff, no weed or anything else. Alcohol kicked my ass once or twice. I could just imagine what cocaine would do. I would be a junkie.
digimon7068
New member
Cal_21 said:
digimon7068
New member
maybe the asshole just doesn't know how to have fun. . .there's lots of peeps out there like that. . .like my pops for instance. . .muh-fugger ain't happy unless he's pissed off about something. . .i'll bet coke wouldn't do shit for him either. . .
DannoMight
New member
your buddy just needs to hit the pipe or start freebasing That oughta do the trick. I could pound lines but it always wore off rather quickly withing a half hour. I could fall asleep within an hr of my last line.
S
Spartacus
Guest
I understand adderal to be 'mixed amphetamine salts' anyhowmyway said:
S
Spartacus
Guest
I needthe amphetiamine for the rest of my bodymyway said:
wtf myway
I can talk until I die
S
Spartacus
Guest
I know where I am
lmao, you are a total KC girl... My dad and his whole family live out bruce springsteen songs, all from Raytown area.myway said:
Tatyana
Elite Mentor
Spartacus said:
Check out zyban. It is stop smoking drug, but off prescription anti-D
You do have to take it continuously.
As far as drugs working or not working on people, this is quite well documented with a number of pharmaceuticals.
The few I remember, anti-depressants only work on 40-60% of people (depending on which type).
I think it is ACE inhibitors (it is some high blood pressure drug) do not work on people of African descent.
There are people who are hyper-metabolisers of codeine, so no pain relief from this drug, similarily for even the common aspirin.
It is all down to our biochemical individuality. We all have the same enzymes and enzyme systems to process drugs, but they function with different efficiencies.
Tatyana
Elite Mentor
Army Vet said:
Looks like cholinergenic receptors play a role.
Neuroscience. 2005;132(4):1159-71.
Blunted response to cocaine in the Flinders hypercholinergic animal model of depression.
Fagergren P, Overstreet DH, Goiny M, Hurd YL.
Karolinska Institute, Department of Clinical Neuroscience, Psychiatry section, Karolinska Hospital, Stockholm, Sweden. [email protected]
The Flinders sensitive line (FSL) rat is a proposed genetic hypercholinergic animal model of human depression. Considering the strong comorbidity between depression and cocaine dependence we investigated the well-documented behavioral and molecular effects of cocaine in the FSL and their control Flinders resistant line (FRL) rats. First, we found no difference between the two lines to establish cocaine self-administration; both lines reached stable responding within 10 days of training at a fixed ratio-1 schedule of reinforcement (1.5 mg/kg/injection). However, the FSL rats exhibited reduced cocaine intake at a dose of 0.09 mg/kg/injection in a within-session dose-response curve (0.02, 0.09, 0.38, 1.5 mg/kg/injection). Second, we examined the effects of repeated cocaine administration on locomotor activity, dopamine overflow and striatal prodynorphin mRNA expression. We found the FSL rats to be low responders to novelty and to exhibit less locomotor activation after repeated cocaine administration (30 mg/kg, i.p., daily injections for 10 days) than their controls. Microdialysis sampling from the nucleus accumbens shell revealed no significant difference in the dopamine overflow between the rat lines, neither during baseline nor after cocaine stimulation. Postmortem analyses of striatal prodynorphin mRNA expression (using in situ hybridization histochemistry) revealed a differentiated response to the cocaine exposure. In contrast to control FRL rats, the FSL rats showed no typical cocaine-evoked elevation of prodynorphin mRNA levels in rostral subregions of the striatum whereas both strains expressed increased prodynorphin mRNA levels in the caudal striatum after cocaine administration. In conclusion, the FSL animal model of depression demonstrates marked blunting of the locomotor and dynorphin neuroadaptative responses to cocaine in accordance with its enhanced cholinergic sensitivity.
Tatyana
Elite Mentor
Also found this which looked quite interesting
http://www.cocaine.org/reward/pleasure.html
Source: University Of Michigan Health System
Date: 2003-01-01
Cocaine Harms Brain's "Pleasure Center", Addict Study Finds; Drug Attacks The Very Cells That Allow Users To Feel Its Effects
ANN ARBOR, MI -- New research results strongly suggest that cocaine bites the hand that feeds it, in essence, by harming or even killing the very brain cells that trigger the "high" that cocaine users feel.
This first-ever direct finding of cocaine-induced damage to key cells in the human brain's dopamine "pleasure center" may help explain many aspects of cocaine addiction, and perhaps aid the development of anti-addiction drugs. It also could help scientists understand other disorders involving the same brain cells, including depression.
The results are the latest from research involving postmortem brain tissue samples from cocaine abusers and control subjects, performed at the University of Michigan Health System and the VA Ann Arbor Healthcare System. The paper will appear in the January issue of the American Journal of Psychiatry. "This is the clearest evidence to date that the specific neurons cocaine interacts with don't like it and are disturbed by the drug's effects," says Karley Little, M.D., associate professor of psychiatry at the U-M Medical School and chief of the VAHS Affective Neuropharmacology Laboratory. "The questions we now face are: Are the cells dormant or damaged, is the effect reversible or permanent, and is it preventable?"
Little and his colleagues report results from 35 known cocaine abusers and 35 non-drug users of about the same age, sex, race and causes of death. Using brain samples normally removed during autopsy, the researchers measured several indicators of the health of the subjects' dopamine brain cells, which release a pleasure-signaling chemical called dopamine. The cells interact directly with cocaine.
The team looked at levels of a protein called VMAT2, as well as VMAT2's binding to a selective radiotracer molecule, and overall dopamine level.
In all three, cocaine users' levels were significantly lower than control subjects. Levels tended to be lowest in cocaine users with depression.
The paper gives the most conclusive evidence yet that dopamine neurons are harmed by cocaine use, because it uses three molecular measures that provide a trustworthy assessment of dopamine neuron health.
Dopamine, Little explains, triggers the actions required to repeat previous pleasures. It's not only involved in drug users' "high" - it helps drive us to eat, work, feel emotions, and reproduce. Normally, when something pleasurable happens, dopamine neurons pump the chemical into the gaps between themselves and related brain cells. Dopamine finds its way to receptors on neighboring cells, triggering signals that help set off pathways to different feelings or sensations.
Then, the dopamine is normally brought back into its home cell, entering through a gateway in the membrane called a transporter. While our brain waits for another pleasurable stimulus - a good meal, a smile from a friend, a kiss - dopamine lies waiting inside the neuron, sequestered in tiny packets called vesicles. VMAT2 acts as a pump to pull returning dopamine into vesicles.
When it comes time for another dopamine release, the vesicles merge with the cell membrane, dumping their contents into the gap, or synapse, and the pleasure signaling process begins again.
Dopamine neurons in the brain's pleasure center die off at a steady rate over a person's lifetime. Severe damage is a hallmark of Parkinson's disease, causing its loss of movement control. "As the words themselves suggest, there's an intimate connection between motion and emotion," says Little. "Emotion puts you in motion -- they're pre-activity preparations. It's not surprising that the basal ganglia, where these dopamine neurons are, is very active in 'emotional states.'"
When first taken, cocaine has a disruptive effect on the brain's dopamine system: It blocks the transporters that return dopamine to its home cell once its signaling job is done. With nowhere to go, dopamine builds up in the synapse and keeps binding with other cells' receptors, sending pleasure signals over and over again. This helps cause the intense "high" cocaine users feel.
Since the dopamine system helps us recognize pleasurable experiences and seek to repeat them, cocaine's long-term dopamine effects likely contribute to the craving addicts feel, and the decreased motivation, stunted emotion and uncomfortable withdrawal they face.
In recent years, many researchers have come to suspect that chronic cocaine use causes the brain to adapt to the drug's presence by altering the molecules involved in dopamine release and reuptake, and in the genetic instructions needed to make those molecules. Little and his colleagues are studying the effects of long-term cocaine use on the brain at a molecular level, in an attempt to explain the effects seen in cocaine users and addicts.
In several studies, including the current one, they've used postmortem samples of brain tissue from known cocaine users who were using the drug at the time of their deaths, and from well-matched control subjects. They focused in on the striatum, an area of the brain with the highest concentration of dopamine neurons.
With approval from the U-M Institutional Review Board and appropriate consent, they interviewed relatives and friends of the subjects, and asked about the subjects' alcohol use, mental illness and other characteristics.
The team previously showed that cocaine users have higher numbers of dopamine transporters, suggesting that the cells tried to make more return gateways to compensate for blocked ones. Recently, they showed in cell cultures that cocaine causes more dopamine transporters to travel from the interior of a cell to the membrane, increasing the overall dopamine uptake level.
The data provide support for the idea that chronic cocaine abuse leads to a phenomenon seen in animals, called allostasis of reward. With extended use of cocaine, the brain's response to the drug is "reset", and drug-taking once pursued for the pleasure it caused becomes drug-taking to avoid the negative feelings associated with the absence of cocaine.
The new data suggest this same phenomenon occurs in human cocaine users, and is quite pronounced at the neurochemical level. The experiment sheds light on the molecular mechanisms involved as dopamine-producing brain cells try to adapt to a cocaine-drenched environment.
VMAT2 protein levels, measured through the use of specific antibodies that bind to the protein, are not as affected by other factors as dopamine transporters are. VMAT2 binding availability, measured through a unique radioactive tracer developed by U-M nuclear medicine specialists, is another assessment of VMAT2 presence and activity. And the overall dopamine level, measured through liquid chromatography, shows how much of the chemical was available at the time of death.
On the whole, all three were significantly lower in cocaine users than in non-drug users. A history of alcohol abuse in cocaine users or controls did not affect the difference significantly.
Levels of VMAT2 protein were lowest in the seven cocaine users with mood disorders that may have been caused by cocaine use. Researchers have found that depressed cocaine users have more severe addiction and mental health problems than non-depressed users. Little hypothesizes that the decreased dopamine vesicles and increased transporters may contribute to cocaine-induced depression and other depressive disorders. This may explain why depressed cocaine users are less likely to respond to some depression treatments.
In all, Little says, "We could be seeing the result of the brain's attempt to regulate the dopamine system in response to cocaine use, to try to reduce the amount of dopamine that's released by reducing the ability to collect it in vesicles. But we could also be seeing real damage or death to dopamine neurons. Either way, this highlights the fragility of these neurons and shows the vicious cycle that cocaine use can create." New treatments will have to break that cycle, he adds, and the new findings may help steer clinical researchers.
He also emphasizes that the vulnerable nature of dopamine neurons is important in understanding the moods and actions of normal adults as they age and lose dopamine neurons naturally. Considerable evidence suggests that uncontained dopamine may be mildly toxic over time.
In future research, Little and his colleagues hope to look for differences in the number of dopamine neurons in the subjects' brain samples, and to study gene activity in the cells of cocaine users and control subjects. They also hope their results will help other researchers study living cocaine users and look for signs of decreased VMAT2 levels.
In addition to Little, the study's authors are David Krolewski, M.S.; Lian Zhang, Ph.D.; and Bader Cassin, M.D. U-M nuclear medicine researcher Kirk Frey, M.D., led the team that developed the radioactive tracer used to measure VMAT2 binding levels. The study was funded by the National Institute on Drug Abuse of the National Institutes of Health, and by a VA Merit Award. Reference: American Journal of Psychiatry 160:1-9, January 2003.
http://www.cocaine.org/reward/pleasure.html
Source: University Of Michigan Health System
Date: 2003-01-01
Cocaine Harms Brain's "Pleasure Center", Addict Study Finds; Drug Attacks The Very Cells That Allow Users To Feel Its Effects
ANN ARBOR, MI -- New research results strongly suggest that cocaine bites the hand that feeds it, in essence, by harming or even killing the very brain cells that trigger the "high" that cocaine users feel.
This first-ever direct finding of cocaine-induced damage to key cells in the human brain's dopamine "pleasure center" may help explain many aspects of cocaine addiction, and perhaps aid the development of anti-addiction drugs. It also could help scientists understand other disorders involving the same brain cells, including depression.
The results are the latest from research involving postmortem brain tissue samples from cocaine abusers and control subjects, performed at the University of Michigan Health System and the VA Ann Arbor Healthcare System. The paper will appear in the January issue of the American Journal of Psychiatry. "This is the clearest evidence to date that the specific neurons cocaine interacts with don't like it and are disturbed by the drug's effects," says Karley Little, M.D., associate professor of psychiatry at the U-M Medical School and chief of the VAHS Affective Neuropharmacology Laboratory. "The questions we now face are: Are the cells dormant or damaged, is the effect reversible or permanent, and is it preventable?"
Little and his colleagues report results from 35 known cocaine abusers and 35 non-drug users of about the same age, sex, race and causes of death. Using brain samples normally removed during autopsy, the researchers measured several indicators of the health of the subjects' dopamine brain cells, which release a pleasure-signaling chemical called dopamine. The cells interact directly with cocaine.
The team looked at levels of a protein called VMAT2, as well as VMAT2's binding to a selective radiotracer molecule, and overall dopamine level.
In all three, cocaine users' levels were significantly lower than control subjects. Levels tended to be lowest in cocaine users with depression.
The paper gives the most conclusive evidence yet that dopamine neurons are harmed by cocaine use, because it uses three molecular measures that provide a trustworthy assessment of dopamine neuron health.
Dopamine, Little explains, triggers the actions required to repeat previous pleasures. It's not only involved in drug users' "high" - it helps drive us to eat, work, feel emotions, and reproduce. Normally, when something pleasurable happens, dopamine neurons pump the chemical into the gaps between themselves and related brain cells. Dopamine finds its way to receptors on neighboring cells, triggering signals that help set off pathways to different feelings or sensations.
Then, the dopamine is normally brought back into its home cell, entering through a gateway in the membrane called a transporter. While our brain waits for another pleasurable stimulus - a good meal, a smile from a friend, a kiss - dopamine lies waiting inside the neuron, sequestered in tiny packets called vesicles. VMAT2 acts as a pump to pull returning dopamine into vesicles.
When it comes time for another dopamine release, the vesicles merge with the cell membrane, dumping their contents into the gap, or synapse, and the pleasure signaling process begins again.
Dopamine neurons in the brain's pleasure center die off at a steady rate over a person's lifetime. Severe damage is a hallmark of Parkinson's disease, causing its loss of movement control. "As the words themselves suggest, there's an intimate connection between motion and emotion," says Little. "Emotion puts you in motion -- they're pre-activity preparations. It's not surprising that the basal ganglia, where these dopamine neurons are, is very active in 'emotional states.'"
When first taken, cocaine has a disruptive effect on the brain's dopamine system: It blocks the transporters that return dopamine to its home cell once its signaling job is done. With nowhere to go, dopamine builds up in the synapse and keeps binding with other cells' receptors, sending pleasure signals over and over again. This helps cause the intense "high" cocaine users feel.
Since the dopamine system helps us recognize pleasurable experiences and seek to repeat them, cocaine's long-term dopamine effects likely contribute to the craving addicts feel, and the decreased motivation, stunted emotion and uncomfortable withdrawal they face.
In recent years, many researchers have come to suspect that chronic cocaine use causes the brain to adapt to the drug's presence by altering the molecules involved in dopamine release and reuptake, and in the genetic instructions needed to make those molecules. Little and his colleagues are studying the effects of long-term cocaine use on the brain at a molecular level, in an attempt to explain the effects seen in cocaine users and addicts.
In several studies, including the current one, they've used postmortem samples of brain tissue from known cocaine users who were using the drug at the time of their deaths, and from well-matched control subjects. They focused in on the striatum, an area of the brain with the highest concentration of dopamine neurons.
With approval from the U-M Institutional Review Board and appropriate consent, they interviewed relatives and friends of the subjects, and asked about the subjects' alcohol use, mental illness and other characteristics.
The team previously showed that cocaine users have higher numbers of dopamine transporters, suggesting that the cells tried to make more return gateways to compensate for blocked ones. Recently, they showed in cell cultures that cocaine causes more dopamine transporters to travel from the interior of a cell to the membrane, increasing the overall dopamine uptake level.
The data provide support for the idea that chronic cocaine abuse leads to a phenomenon seen in animals, called allostasis of reward. With extended use of cocaine, the brain's response to the drug is "reset", and drug-taking once pursued for the pleasure it caused becomes drug-taking to avoid the negative feelings associated with the absence of cocaine.
The new data suggest this same phenomenon occurs in human cocaine users, and is quite pronounced at the neurochemical level. The experiment sheds light on the molecular mechanisms involved as dopamine-producing brain cells try to adapt to a cocaine-drenched environment.
VMAT2 protein levels, measured through the use of specific antibodies that bind to the protein, are not as affected by other factors as dopamine transporters are. VMAT2 binding availability, measured through a unique radioactive tracer developed by U-M nuclear medicine specialists, is another assessment of VMAT2 presence and activity. And the overall dopamine level, measured through liquid chromatography, shows how much of the chemical was available at the time of death.
On the whole, all three were significantly lower in cocaine users than in non-drug users. A history of alcohol abuse in cocaine users or controls did not affect the difference significantly.
Levels of VMAT2 protein were lowest in the seven cocaine users with mood disorders that may have been caused by cocaine use. Researchers have found that depressed cocaine users have more severe addiction and mental health problems than non-depressed users. Little hypothesizes that the decreased dopamine vesicles and increased transporters may contribute to cocaine-induced depression and other depressive disorders. This may explain why depressed cocaine users are less likely to respond to some depression treatments.
In all, Little says, "We could be seeing the result of the brain's attempt to regulate the dopamine system in response to cocaine use, to try to reduce the amount of dopamine that's released by reducing the ability to collect it in vesicles. But we could also be seeing real damage or death to dopamine neurons. Either way, this highlights the fragility of these neurons and shows the vicious cycle that cocaine use can create." New treatments will have to break that cycle, he adds, and the new findings may help steer clinical researchers.
He also emphasizes that the vulnerable nature of dopamine neurons is important in understanding the moods and actions of normal adults as they age and lose dopamine neurons naturally. Considerable evidence suggests that uncontained dopamine may be mildly toxic over time.
In future research, Little and his colleagues hope to look for differences in the number of dopamine neurons in the subjects' brain samples, and to study gene activity in the cells of cocaine users and control subjects. They also hope their results will help other researchers study living cocaine users and look for signs of decreased VMAT2 levels.
In addition to Little, the study's authors are David Krolewski, M.S.; Lian Zhang, Ph.D.; and Bader Cassin, M.D. U-M nuclear medicine researcher Kirk Frey, M.D., led the team that developed the radioactive tracer used to measure VMAT2 binding levels. The study was funded by the National Institute on Drug Abuse of the National Institutes of Health, and by a VA Merit Award. Reference: American Journal of Psychiatry 160:1-9, January 2003.
S
Spartacus
Guest
yesmyway said:
stosstruppe
Well-known member
Smurfy said:
+1
My mum smoked 20-30 a day for 30-35 years and went cold turkey using Zyban about 5 years ago. She said the night sweats were bad initially but was worth it long term.
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