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From: "Steve Harris" <>
Subject: Re: Ziban
Date: Tue, 11 Jun 2002 17:00:37 -0700
Message-ID: <ae636s$qvd$>

CBI <> wrote in message ...
>"Steve Harris" <> wrote in message
>> CBI <> wrote in message ...
>> ><> wrote in message
>> >
>> >>
>> >> Wellbutrin is stimulant type anti depressant.
>> >
>> >Gail,
>> >
>> >You have no idea what you are talking about. Wellbutrin/Zyban is not speed.
>> >
>> >--
>> >CBI, MD
>> She didn't say it was.
>Sure she did.

Yes, someone pointed out the other message.

>> She said it's a stimulant type antidepressant, and so
>> it is.  Why do you think it's a seizure risk?  Read the PDR (or your Drugdex
>> or Nat Med Formulary or whatever you use) on the stuff.
>If you say so. It really does not stand out in this regard.


Read the experimental literature. It surely DOES stand out in this regard.
It's been used as a dopaminergic probe in drug models for years. It's not
amphetamine, but it has some similarities in action, cross tolerance, and
induction of self-administrative behavior. No, the manufacturers don't
really play this up much. To me it quacks (weakly) like a duck.

Exp Clin Psychopharmacol 1998 Feb;6(1):32-44

Discriminative-stimulus and participant-rated effects of methylphenidate,
bupropion, and triazolam in d-amphetamine-trained humans.

Rush CR, Kollins SH, Pazzaglia PJ.  Department of Psychiatry and Human
Behavior, University of Mississippi Medical Center, Jackson 39219-4505,

The discriminative-stimulus and participate-rated effects of a range of
doses of d-amphetamine (2.5-20 mg), methylphenidate (5-40 mg), bupropion
(50-400 mg), and triazolam (0.0625-0.5 mg) were tested in 5 humans
trained to discriminate between oral d-amphetamine (20 mg) and placebo.
d-Amphetamine and methylphenidate generally dose dependently increased
drug-appropriate responding. Bupropion and triazolam on average
occasioned less than or equal to 40% drug-appropriate responding.
d-Amphetamine, methylphenidate, and bupropion produced stimulant-like
participant-rated effects, while triazolam produced sedative-like
effects. These results further demonstrate that the acute behavioral
effects of d-amphetamine and methylphenidate overlap extensively in
humans, which is concordant with preclinical studies. Bupropion produced
some d-amphetamine-like, participant-rated drug effects but did not
occasion significant levels of d-amphetamine-appropriate responding.
These findings are concordant with previous findings of a dissociation
between the discriminative-stimulus and participant-rated effects of

Publication Types: Clinical Trial
PMID: 9526144 [PubMed - indexed for MEDLINE]

Psychopharmacology (Berl)  1997 Nov;134(2):201-12

Dopaminergic mediation of the discriminative stimulus effects of
bupropion in rats.

Terry P, Katz JL.  Psychobiology Section, NIDA Intramural Research
Program, National Institutes of Health, Baltimore, MD 21224, USA.

Bupropion is a novel, non-tricyclic antidepressant with a primary
pharmacological action of monoamine uptake inhibition. The drug resembles
a psychostimulant in terms of its neurochemical and behavioural profiles
in vivo, but it does not reliably produce stimulant-like effects in
humans at clinically prescribed doses. Bupropion binds with modest
selectivity to the dopamine transporter, but its behavioural effects have
often been attributed to its inhibition of norepinephrine uptake. This
experiment examines monoaminergic involvement in the discriminative
stimulus effects of bupropion. Rats were trained to press one lever when
injected i.p. with bupropion (17.0 mg/kg), and another lever when
injected with saline. In substitution tests, dose-response curves were
obtained for several monoamine uptake inhibitors. Nine of ten dopamine
uptake blockers fully substituted for bupropion; the exception,
indatraline (LU 19-005), partially substituted (71% bupropion-appropriate
responding). Serotonin and norepinephrine uptake blockers (zimelidine and
nisoxetine, respectively) produced negligible or limited substitution,
and the anti-muscarinic dopamine uptake blocker benztropine produced
limited partial substitution. A series of dopamine D1-like and D2-like
receptor agonists were also tested: only the D2-like agonist RU 24213
fully substituted; three other D2-like agonists and four D1-like agonists
partially substituted (50% < drug responding < 80%). Antagonism of the
discriminative effects of bupropion was obtained with a D1- and a D2-like
dopamine antagonist. The results demonstrate strong similarities with
those obtained using other dopamine uptake inhibitors as training drugs,
and support the view that the behavioural effects of bupropion are
primarily mediated by dopaminergic mechanisms.  PMID: 9399385 [PubMed -
indexed for MEDLINE]

J Pharmacol Exp Ther  1989 Oct;251(1):150-5
Effects of cocaine and related drugs in nonhuman primates. III.
Self-administration by squirrel monkeys.

Bergman J, Madras BK, Johnson SE, Spealman RD.  Department of Psychiatry,
Harvard Medical School, New England Regional Primate Research Center,
Southborough, Massachusetts.

The self-administration of cocaine was compared with that of bupropion,
mazindol, methylphenidate and nomifensine, drugs that displace
[3H]cocaine from its binding sites and have monoamine uptake inhibiting
effects in common with those of cocaine. Squirrel monkeys responded under
a second-order fixed-interval schedule of consequent i.v. drug injection,
and dose-effect curves were established by determining stable rates of
responding maintained by saline and a range of doses of each drug.
Cocaine (0.01-0.56 mg/kg/injection), bupropion (0.1-3.0 mg/kg/injection),
phenylpropyl)piperazine-(0.03-1.0 mg/kg/injection), methylphenidate
(0.01-0.3 mg/kg/injection) and nomifensine (0.01-0.3 mg/kg) maintained
comparable rates and patterns of responding in all subjects, whereas
mazindol (0.03-0.3 mg/kg) maintained self-administration behavior in only
half the monkeys studied.  The present results in conjunction with those
of previous studies in squirrel monkeys reveal a close correspondence
between the relative potencies of cocaine and related drugs for
maintaining i.v. self-administration and for increasing rates of
schedule-controlled responding, suggesting that the reinforcing and
psychomotor-stimulant effects of the drugs are mediated similarly. The
potency relations observed in the present study also agree generally with
those observed for displacement of specifically bound [3H]cocaine in
monkey caudate-putamen suggesting that the reinforcing effects of cocaine
involve its actions at specific recognition sites in brain.PMID: 2529365
[PubMed - indexed for MEDLINE]

J Addict Dis  2002;21(2):1-16

Bupropion treatment for cocaine abuse and adult attention-deficit/hyperactivity

Levin FR, Evans SM, McDowell DM, Brooks DJ, Nunes E.
Department of Psychiatry, Columbia University/New York State Psychiatric
Institute, New York 10032, USA.

There are few published studies assessing the efficacy of pharmacologic
treatments for attention-deficit hyperactivity disorder (ADHD) among
substance abusers seeking treatment. Eleven patients who met DSM-IV
diagnostic criteria for cocaine dependence and adult ADHD were entered
into a 12-week single-blind trial of divided daily doses of bupropion
(BPR). All patients received weekly individual standardized relapse
prevention therapy. Treatment compliance and retention were good.
Patients reported significant reductions in attention difficulties,
hyperactivity and impulsivity. Self-reported cocaine use, cocaine
craving, and cocaine positive toxicologies, also decreased significantly.
In a previously published trial, 12 patients who met similar diagnostic
criteria for adult ADHD and cocaine dependence were entered into a
12-week trial of divided daily doses of sustained-release methylphenidate
(MPH). Improvements observed on BPR were similar to, and did not differ
from those previously observed with MPH.  These preliminary data suggest
that BPR may be as effective as sustained-release MPH, when combined with
relapse prevention therapy, for cocaine abusers with adult ADHD. However,
a future study directly comparing BPR to MPH in a double-blind
placebo-controlled trial is needed.  PMID: 11916368 [PubMed - in process]


Eur J Pharmacol  2002 May 17;443(1-3):113-8
Nicotine and bupropion share a similar discriminative stimulus effect.
Young R, Glennon RA.

Department of Medicinal Chemistry, School of Pharmacy, Box 980540, Virginia
Commonwealth University, 23298-0540, Richmond, VA, USA

Bupropion is a weakly potent central nervous system (CNS) stimulant that
is marketed both as an antidepressant and as an anti-smoking aid. The
mechanism(s) by which it produces its effects is not well understood. In
the present study, the effect of bupropion was examined in rats trained
to discriminate the stimulus effect of 0.60 mg/kg of (-)-nicotine from
saline in a two-lever drug discrimination task. In tests of stimulus
generalization (substitution), the nicotine (ED(50)=0.17 mg/kg) stimulus
completely generalized to bupropion (ED(50)=5.50 mg/kg). In addition,
interaction studies were conducted that evaluated the effect of 3.0 mg/kg
of bupropion, a dose that when given alone produced saline-appropriate
responding, in combination with various doses of nicotine. This
application resulted in an enhancement of the potency of nicotine
(ED(50)=0.05 mg/kg), as indicated by a leftward shift of the nicotine
dose-effect function. In tests of stimulus antagonism, various doses of
bupropion were administered prior to the training dose of nicotine and
were found to be ineffective as antagonists of the nicotine stimulus. In
contrast, the nicotinic acetylcholine receptor (nicotine receptor)
antagonist mecamylamine (AD(50)=0.40 mg/kg) completely blocked the
stimulus effect of nicotine.  Mecamylamine did not attenuate the stimulus
generalization of bupropion. The results demonstrated that bupropion can
produce a nicotine-like response in nicotine-trained animals, but it does
so via a mechanism of action that is unlike that of nicotine. It is
speculated that bupropion may be somewhat effective as an anti-smoking
treatment in people who are motivated to quit smoking because low doses
of bupropion produce a nicotine-like effect(s) that serve as a suitable
substitute for nicotine.PMID: 12044800 [PubMed - in process]


Sleep Res Online  1998;1(1):49-61

Increased dopaminergic transmission mediates the wake-promoting effects
of CNS stimulants.

Nishino S, Mao J, Sampathkumaran R, Shelton J.  Stanford University
School of Medicine, Sleep Disorders Center, Palo Alto, CA 94304, USA.

Amphetamine-like stimulants are commonly used to treat sleepiness in
narcolepsy.  These compounds have little effect on rapid eye movement
(REM) sleep-related symptoms such as cataplexy, and antidepressants
(monoamine uptake inhibitors) are usually required to treat these
symptoms. Although amphetamine-like stimulants and antidepressants
enhance monoaminergic transmission, these compounds are non-selective for
each monoamine, and the exact mechanisms mediating how these compounds
induce wakefulness and modulate REM sleep are not known. In order to
evaluate the relative importance of dopaminergic and noradrenergic
transmission in the mediation of these effects, five dopamine (DA) uptake
inhibitors (mazindol, GBR-12909, bupropion, nomifensine and amineptine),
two norepinephrine (NE) uptake inhibitors (nisoxetine and desipramine),
d-amphetamine, and modafinil, a non-amphetamine stimulant, were tested in
control and narcoleptic canines. All stimulants and dopaminergic uptake
inhibitors were found to dose-dependently increase wakefulness in control
and narcoleptic animals. The in vivo potencies of DA uptake inhibitors
and modafinil on wake significantly correlated with their in vitro
affinities to the DA and not the NE transporter. DA uptake inhibitors
also moderately reduced REM sleep, but this effect was most likely
secondary to slow wave sleep (SWS) suppression, since selective DA uptake
inhibitors reduced both REM sleep and SWS proportionally. In contrast,
selective NE uptake inhibitors had little effect on wakefulness, but
potently reduced REM sleep. These results suggest that presynaptic
activation of DA transmission is critical for the pharmacological control
of wakefulness, while that of the NE system is critical for REM sleep
regulation. Our results also suggest that presynaptic activation of DA
transmission is a key pharmacological property mediating the
wake-promoting effects of currently available CNS stimulants.  PMID:
11382857 [PubMed - indexed for MEDLINE]

I welcome email from any being clever enough to fix my address. It's open
book.  A prize to the first spambot that passes my Turing test.

From: ((Steven B. Harris))
Date: 12 Jun 2002 17:18:54 GMT
Subject: Re: Ziban
Message-ID: <>

>>> Read the experimental literature.
>>I read your citations. The gist I get from it is that it is weak in this
>>regard. I'm not impressed.
>Try taking it at night..


Try taking it *at all*.  Again my criticism that most doctors would be a lot
better doctors if they actually tried taking THEMSELVES any and all drugs they
prescribe, just for a day or two.  (Note to anethesiologists-- no, stay away
from fentenyl; every rule has a few exceptions).

Note sources say Wellbutrin/Ziban isn't a *reliable* simulant at therapeutic
doses.  The qualification is that it's a pretty reliable if you take more than
you're supposed to. Which some people will. Cases of bupropion recreational use
have been reported.


Steve Harris

From: "Steve Harris" <>
Subject: Re: Ziban
Date: Wed, 12 Jun 2002 16:16:21 -0700
Message-ID: <ae8kpk$pa6$>

Kurt Ullman wrote in message ...
>>Note sources say Wellbutrin/Ziban isn't a *reliable* simulant at
>>therapeutic doses.  The qualification is that it's a pretty reliable if
>>you take more than you're supposed to. Which some people will. Cases of
>>bupropion recreational use have been reported.
>       There have also been reports of recreational use of Haldol. I knew a
>junkie that used to grind up Contact's little tiny time pills and inject it
>for cheap barb high. Thusly, I am less than impressed with most reports of
>recreational use. Seems that almost anything can be abused recreationally.

I knew somebody was going to say that. Which is why I recommend you try the
stuff for yourself. It's not a controlled substance. Get some doc to write
you scrip for 20 or 30.  Tell him you're trying to quit cocaine.

I welcome email from any being clever enough to fix my address. It's open
book.  A prize to the first spambot that passes my Turing test.

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