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500 Things to Do After Snorting Quetiapine

The question still hasn't been answered. Seroquel obviously has somthing to it or it wouldn't be abused- it's that simple.

Regardless of whether it's a "real" drug or it makes some dysphoric, somehow it can get some people high. I'm still curious to as the original question...
 
i have like 2 bottles of seroquil and it never made me unusally tired. it just made it to where i could sleep a couple hours after i took it. and even after i got off of it i didnt have any manic/depressive episodes. i was diagnosed as bipolar the day after i started detoxing off of a 40 pill+a day habit. i never tohught it was anything worth doing anything with.
 
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500 Things to Do After Snorting Quetiapine


Slap yourself across the head for snorting an antipsychotic believing it'd be like coke! =D
 
Perhaps this thred should be renamed : -

"Anything you have tried to do whilst under the influence of a heavy dose of a major tranquilizer!"

Google: 'Quetiapine' or 'Seroquel' --- buy some and then us know!
 
The question still hasn't been answered. Seroquel obviously has somthing to it or it wouldn't be abused- it's that simple.

Regardless of whether it's a "real" drug or it makes some dysphoric, somehow it can get some people high. I'm still curious to as the original question...

Part of the problem is the absurdity of the whole matter, the lack of (appropriate) self-administration studies and the fact that it all seems to come piecemeal, in the form of case studies, maybe even from the maker of aripiprazole, the maker of asenapine or even qtp's maker, which is about to lose its patent. I'd like to sodomize Missy Monroe. The only physiologically-rigorous examination of qtp's abuse potential I know of is still in press (I link to it in the first post). Otherwise I turn up stuff like this:

The article focuses on the addictive potential of quetiapine (Seroquel). It cites the case of a 29-year-old man who presented a walk-in at a clinic claiming a diagnosis of schizophrenia. According to the article, a pharmacy review determined that the man had been filling multiple prescriptions for quetiapine from several sources when found to be sedated. It states that federal regulators could be prompted to declare the drug a controlled substance if the current misuse of quetiapine continues.

which glosses an item in Brown University's Psychopharmacology Update, September 2008.
 
I tried to use it to kill a heavy DOI trip.. yuck.

Akathisia whilst tripping balls, sedated as hell but no hope of sleeping. Tried at 100mg with very little effect, tried another 100mg. Almost called an ambulance it was so fucking bad.

A mate says 25mg is a better dose for sleeping after amphetamines

I dont think I could bring myself to touch it ever again.
 
lol here we go again...

i was trying to figure out why people abuse seroquel a few months ago. i did find some cases of abuse in the medical literature, but nothing really substantial. anyway, i read in one paper that it had something to do with histamine receptors and their effects on dopamine. ill try and dig it up.

here *nevermind, the op links to this article*
NSFW:

Review
The role of antihistaminic effects in the misuse of quetiapine: A case report and review of the literature

Bernard A. Fischera, b, Corresponding Author Contact Information, E-mail The Corresponding Author and Douglas L. Boggsa

aMaryland Psychiatric Research Center, University of Maryland School of Medicine, Baltimore, USA

bVeterans Affairs Capital Network (VISN 5) Mental Illness Research, Education, and Clinical Center (MIRECC), Baltimore, USA
Received 22 July 2009;
revised 28 October 2009;
accepted 2 November 2009.
Available online 6 November 2009.

Abstract

Recent case reports and case series suggest that the atypical antipsychotic quetiapine has the potential for misuse. This includes drug-seeking behaviors motivated by quetiapine as well as inappropriate (intranasal or intravenous) administration. We present an additional case of quetiapine misuse and review other published cases. In general, quetiapine misuse is associated with prior CNS depressant use and is more common in forensic settings. The mechanism of reinforcement for this misuse is unknown, but we hypothesize that it is related to quetiapine's pharmacological profile as an antihistamine with a relative low affinity for dopamine receptors. The risks to individuals and society of exaggerating/simulating symptoms to obtain high-dose quetiapine in the absence of a clinical indication are discussed. This includes the unwelcome possibility of restricting access to this effective medication.

Keywords: Quetiapine; Antipsychotic; Substance misuse; Substance abuse; Antihistamine
Article Outline

1. Introduction
2. Case report
3. Review of the literature
4. Possible mechanism
5. Risks of quetiapine misuse
6. Conclusion
References

1. Introduction
Prescription medications are misused if they are taken in a way other than as prescribed or if symptoms are invented or exaggerated in order to acquire a prescription. No medication is completely harmless and patients can be put at significant risk by misuse of medications. This article presents the case of a patient embellishing symptoms in an attempt to obtain increased doses of the atypical antipsychotic quetiapine. Following the case, we review the literature on quetiapine misuse and discuss possible mechanisms underlying the phenomenon. We conclude with a consideration of the risks of unrecognized quetiapine misuse to individuals and to society at large.

2. Case report

Mr. A was a married, employed, white 53-year-old male. He presented with several weeks of depressed mood following a third arrest for driving while intoxicated (DWI). At intake, he denied any discrete periods of elevated, expansive, or irritable mood, sleeplessness, grandiosity, pressured speech (observed by family or friends), racing thoughts or increased goal-directed behavior. Despite the 3 arrests, Mr. A denied regular alcohol use and his laboratory results (including liver function tests and complete blood count) were within normal limits. Mr. A did report a history of compulsive gambling, which had left him in significant debt. He had never been seen by a psychiatrist or counselor and had never been prescribed any psychotropics. He was started on duloxetine and his mood improved.

Mr. A was extremely intelligent and began investigating a not-criminally responsible defense. As his hearing approached, he began reporting recollections of symptoms consistent with previous manic episodes. In contrast to his evaluation visits, he now reported his gambling had come in discrete periods coupled with euphoric mood. He also began reporting the events of the DWI differently making a point of saying he was “manic” when he was stopped that night. Because there was some clinical doubt as to Mr. A's true diagnosis, and duloxetine monotherapy put him at theoretical risk for mood instability, he was started on quetiapine.

Mr. A was allowed to serve his DWI sentence part-time several days/week. He continued to attend the clinic. During his sessions he began pressing for higher and higher doses of quetiapine. Rather than experiencing relief after dose increases, he reported worsening irritability and insomnia. He was finally presented the option of switching to a different mood-stabilizing agent. He then acknowledged quetiapine made him feel “dreamy” and reported he was trying to get the dose high enough that he could “sleep through” his incarceration.
3. Review of the literature

A search of PubMed using the string “quetiapine AND (abuse OR dependence OR misuse OR addiction)” yielded eight published case reports/case series of quetiapine misuse in English ([Chen et al., 2009], [Hussain et al., 2005], [Morin, 2007], [Murphy et al., 2008], [Paparrigopoulos et al., 2008], [Pinta and Taylor, 2007], [Reeves and Brister, 2007] and [Waters and Joshi, 2007]) as well as a letter describing a general misuse phenomenon in Los Angeles County Jail (Pierre et al., 2004); see Table 1.
Table 1.

Summary of case reports of quetiapine misusea.
Reference Sex Race Age Diagnosis (non-substance related) Prior addictive behavior Route of administration Comments
Fischer and Boggs (present report) M W 53 Mood disorder not otherwise specified Yes (alcohol abuse, gambling) Oral Related to incarceration
Hussain et al. (2005) F – 34 Borderline personality disorder, depressive episodes Yes (polysubstance dependence) Intranasal; IV Related to incarceration
Morin (2007) F W 28 Schizoaffective disorder (bipolar type) Yes (polysubstance abuse) Intranasal Court-ordered hospitalization
Waters and Joshi (2007) M W 33 – Yes (polysubstance dependence) IV with cocaine Combination reported as “hallucinogenic”
Pinta and Taylor (2007) M – 39 Generalized anxiety disorder Yes (opiate abuse) Unreported (oral assumed) Related to incarceration
Reeves and Brister (2007) M – 49 None Yes (alcohol dependence, benzodiazepine abuse) Unreported (oral assumed) Urine being monitored after multiple DUIs
Reeves and Brister (2007) M – 23 None Yes (benzodiazepine dependence) Unreported (oral assumed) Stole quetiapine from girlfriend with schizophrenia
Reeves and Brister (2007) M – 39 Bipolar disorder – Unreported (oral assumed) Outpatient misuse
Paparrigopoulos et al. (200 M – 48 Generalized anxiety disorder; “depressive reaction” Yes (alcohol dependence, benzodiazepine dependence) Oral with benzodiazepines Reported to augment benzodiazepine feeling; preferred to alcohol
Murphy et al. (200 M W 29 Probable malingering None known (negative urine toxicology) Oral Outpatient misuse
Chen et al. (2009) F – 59 Bipolar disorder Yes (concurrent benzodiazepine dependence) Unreported (oral assumed) Outpatient misuse
Pierre et al. (2004) – – – – Yes Oral; intranasal Report of widespread misuse in Los Angeles County Jail
Full-size table
a M: male, F: female; W: White, Caucasian; DO: disorder; IV: intravenous; DUI: driving while under the influence; “–” indicates information not reported or not applicable.

View Within Article


Reports of quetiapine misuse include taking the medication intravenously ([Hussain et al., 2005] and [Waters and Joshi, 2007]) or intranasally ([Hussain et al., 2005], [Morin, 2007] and [Pierre et al., 2004]), taking excessive amounts ([Chen et al., 2009], [Murphy et al., 2008], [Paparrigopoulos et al., 2008] and [Reeves and Brister, 2007]), malingering symptoms to obtain the drug ([Murphy et al., 2008] and [Reeves and Brister, 2007]), and acquiring/selling quetiapine “on the street”([Murphy et al., 2008], [Pierre et al., 2004], [Pinta and Taylor, 2007] and [Reeves and Brister, 2007]). When the effect of quetiapine is described, it is often similar to the effect described by Mr. A, i.e. “dreamy”, calming, or soporific ([Chen et al., 2009], [Hussain et al., 2005], [Morin, 2007], [Paparrigopoulos et al., 2008], [Pierre et al., 2004], [Pinta and Taylor, 2007] and [Reeves and Brister, 2007]). Only one report describes a “hallucinogenic” effect, but this was in response to an intravenous quetiapine and cocaine combination (Waters and Joshi, 2007). Street slang for quetiapine includes “Susie-Q”(Pinta and Taylor, 2007), “baby-heroin”(Waters and Joshi, 2007), and “quell” (Pierre et al., 2004). The intravenous combination of quetiapine and cocaine is referred to as “Q-Ball” in one report (although it is unclear if this is street slang or a label from the authors (Waters and Joshi, 2007)).

In most cases, misuse of quetiapine was connected to a forensic setting such as incarceration (including the present report ([Hussain et al., 2005], [Pierre et al., 2004] and [Pinta and Taylor, 2007])), court-ordered hospitalization (Morin, 2007), or other oversight by the legal system (e.g. monitoring urines (Reeves and Brister, 2007)). In almost every report, the person misusing quetiapine is described as having a prior drug or alcohol problem. Prior drug misuse was mainly polysubstance abuse/dependence or problems with opiates, alcohol, or benzodiazepines ([Hussain et al., 2005], [Morin, 2007], [Paparrigopoulos et al., 2008], [Pinta and Taylor, 2007], [Reeves and Brister, 2007] and [Waters and Joshi, 2007]). Quetiapine does not seem to be substitute for more activating drugs such as cocaine or amphetamines.
4. Possible mechanism

The reinforcing properties of quetiapine have not been examined in human or non-human behavioral research, but its pharmacology suggests two plausible explanations for its misuse. Although it was initially believed quetiapine had minimal anticholinergic activity (Goldstein and Brecher, 2000 J.M. Goldstein and M. Brecher, Clarification of anticholinergic effects of quetiapine, J. Clin. Psychiatry61 (2000), p. 680. View Record in Scopus | Cited By in Scopus (1)Goldstein and Brecher, 2000), trials of high-dose quetiapine have demonstrated anticholinergic effects in humans ([Boggs et al., 2008] and [Pierre et al., 2005]) and there are multiple case reports of anticholinergic drug abuse/misuse in the literature ([Buhrich et al., 2000], [Hidalgo and Mowers, 1990], [Land et al., 1991] and [Pullen et al., 1984]). However, these reports have almost uniformly described anticholinergic intoxication as euphoric and stimulatory. This does not fit the clinical description of quetiapine's effects, which more closely resemble central nervous system depressants (Tcheremissine, 200. Quetiapine has a high antagonistic affinity for the histamine H1 receptor; especially in relationship to its antagonistic affinity for the D2 receptor (Kroeze et al., 2003). These antihistaminic effects offer a more likely explanation for the misuse/abuse potential of quetiapine.

Several reports have shown antihistamines are misused in humans ([Bailey and Davies, 2008], [Halpert et al., 2002] and [Thomas et al., 2009]), but the exact mechanism behind their reinforcing properties has not been clearly explained. In rodent studies, peripheral administration of antihistamines increases dopamine release in the ventral striatum (Dringenberg et al., 199 and substances with an abuse potential, no matter what their mechanism of action, enhance excitatory neurons of midbrain dopaminergic neurons (Saal et al., 2003). Also, lesions of the rostroventral tuberomammillary nucleus, the histamine-producing area of the brain, increase rewarding self-stimulatory behavior in rats (Wagner et al., 1993). This suggests histamine has an inhibitory effect on the reward system. The reinforcing effects of antihistamines could be a result of disinhibition of a primed reward system. This may explain why misuse of quetiapine and other antihistamines have largely been reported in people with a previous history of substance abuse. Substance abuse increases long-term potentiation of the reward system (Saal et al., 2003) and a hyperactive reward system may be necessary for antihistaminic medications to have a reinforcing effect.

People with a history of sedative abuse have ranked antihistamines significantly higher on “liking” versus placebo (Preston et al., 1992) and not significantly different from the benzodiazepine lorazepam (Mumford et al., 1996). Whether the reinforcing properties for antihistamines would be similar among people with a history of stimulant abuse is not known, but the majority of antihistamine and quetiapine misuse cases are among people who report previous use of CNS depressants.

Behavioral studies in non-human primates have found antihistamines can maintain responses in cocaine-conditioned animals ([Bergman and Spealman, 1986] and [Sannerud et al., 1995]) and lead to motor excitation (Evans and Johanson, 1989). In contrast, the effect of antihistamines in humans is calming or sedating. The difference of effect between non-human primates and humans may indicate divergent reinforcing mechanisms and perhaps a limited relevance of animal models.

Other antipsychotics (e.g. clozapine, olanzapine, and chlorpromazine) also have antihistaminic effects, but have not been linked to have high abuse potential. Why would quetiapine have a higher abuse potential than other antihistaminic antipsychotics? One answer is the superior safety profile of quetiapine for side effects, especially movement disorders (Farah, 2005). The rarity of dystonia and extrapyramidal side effects may make quetiapine a more attractive option for misuse compared to other antipsychotics. Quetiapine has a low affinity for and quickly dissociates from dopamine receptors ([Kapur and Seeman, 2000] and [Tauscher et al., 2004]). Dopamine is another important molecule in reward circuitry. High dopamine D2 receptor antagonism in humans is correlated with antipsychotic-induced dysphoria (Mizrahi et al., 2007) and rodent data shows dopamine D1 antagonism abolishes the antihistaminic potentiation of other substances of abuse ([Suzuki et al., 1990] and [Suzuki et al., 1991]). Quetiapine, due to its low affinity and fast disassociation from both D1 and D2 receptors ([Kapur and Seeman, 2000] and [Tauscher et al., 2004]), may have less potential to disrupt any reinforcing antihistaminic effects.
5. Risks of quetiapine misuse

Side effects of atypical antipsychotics such as quetiapine are not benign and can include metabolic disturbances such as weight gain and glucose intolerance (ADA, 2004). Although quetiapine-induced movement disorders are extremely rare, there has been at least one reported case of resulting tardive dyskinesia (Rizos et al., 2007). Individuals without a primary psychotic disorder may be at increased risk for antipsychotic-induced movement disorders including tardive dyskinesia (Kane, 1999). Exposure to antipsychotics, as with any medication, should be limited to those individuals with a clinical indication.

In addition to personal risks, quetiapine misuse has harmful implications for society. Atypical antipsychotics are expensive drugs. Providing quetiapine to malingering individuals in forensic settings effects mental health budgets in these institutions, which ultimately rely on public resources. Murphy et al. (200 also point out that injudicious prescription of quetiapine may cause tighter federal regulations over the drug including possible schedule as a controlled substance. This, in turn, would present obstacles in getting the medication to people who truly need it.
6. Conclusion

Quetiapine occupies a distinct place in the pharmacopoeia and needs to be available to treat the individualized needs of people with psychiatric disorders. However, some individuals will embellish or simulate symptoms in order to get the medication inappropriately. The misuse potential of quetiapine is likely related to its histaminic blockade coupled with its comparatively mild action at dopamine receptors. Accordingly, quetiapine substitutes for sedating agents and individuals with a history of alcohol, benzodiazepine, or opiate abuse are particularly at risk. Misuse is increased in forensic settings, although the phenomenon is not restricted to this situation. Given individual and societal dangers, the potential for quetiapine misuse should be recognized and should factor into clinical decision-making.
References

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Corresponding Author Contact InformationCorresponding author at: Maryland Psychiatric Research Center, University of Maryland School of Medicine, Psychiatry, P.O. Box 21047, 55 Wade Avenue, Baltimore, MD 21228, USA. Tel.: +1 410 402 7113; fax: +1 410 402 7198.

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Uh...guys, there's no mystery here. Quetiapine is one of the go-to psychotropic meds these days, both as an antipsychotic and for off-label purposes. It's a relatively low-affinity dopamine antagonist with proportionally higher affinity for the H1 receptor than others, giving it a highly sedating quality that makes it attractive to cynical authority figures [prison staff], professionals [weary doctors in psych wards], and the largely uneducated populace to whom these drugs are catered in the first place - schizophrenics, rapidly cycling manic-depressives, and fucked up jailbirds who won't shut up. I think the right question to ask is, "Who among this largely homogeneous group would not try to abuse such a highly sedating, borderline narcotizing substance were they to get the chance?"

For christ's sake, these people don't know what the fucking basal ganglia is, nor have they ever heard of a 'dopaminergic mesolimibic reward pathway' implicated in the rewarding properties of most drugs of abuse. Further, these people have no idea (nor do they care) that the very extracellular G-protein coupled receptor sites whose binding by dopamine is necessary to initiate the intracellular signaling cascade that ultimately culminates in the downstream experience of salient pleasure is actually clogged up by this molecule. They really don't give a shit. To an uneducated, psychotic, incarcerated compulsive drug seeker, quetiapine is fundamentally no different than a barbiturate, a shitty opioid, or even fucking Benadryl. Most of these people aren't intelligent, 'sophisticated' poly-drug users interested in refining and maximizing a high, or pushing the boundaries of consciousness, or even seeking novelty. They are not attuned to the subtleties of altered states of consciousness. Most of these people would never show up on a board like this, let alone concern themselves with what they're actually taking. They're just trying to get fucked up.

Quetiapine, in its popularity, just happens to be the compound that got the most attention, the most case reports, the most hysteria. That is all.

I'd like to sodomize Missy Monroe

Yes.
 
I used to take that shit. Never snorted it though. It didn't feel fun. Just made me extremely tired.
 
onmyway, thanks for the find.

P A said:
...the very extracellular G-protein coupled receptor sites whose binding by dopamine is necessary to initiate the downstream experience of salient pleasure is actually clogged up by this molecule

The urge to go into HELLO MCFLY mode is strong here. We give pharmacologically-sound reasons for why a quetiapine abuser cannot possibly be enjoying himself, because the substance precludes enjoyment altogether.

But the case studies converge. A confluence of behavior presents itself. How do we interpret the pattern of drug-seeking that seems to be specific to quetiapine? It is a paradox. Enjoyability is a necessary condition for self-reinforcement (this is a priori). Dysphoria provokes aversion and aversion is negative reinforcement.

Dr. Fischer attempts to resolve this paradox in a clever way. I think it's important to consider his argument as a plausible mechanism for quetiapine self-reinforcement:

Fischer said:
...substances with an abuse potential, no matter what their mechanism of action, enhance excitatory neurons of midbrain dopaminergic neurons (Saal et al., 2003). Also, lesions of the rostroventral tuberomammillary nucleus, the histamine-producing area of the brain, increase rewarding self-stimulatory behavior in rats (Wagner et al., 1993). This suggests histamine has an inhibitory effect on the reward system. The reinforcing effects of antihistamines could be a result of disinhibition of a primed reward system [primer: any igniter that is used to initiate the burning of a propellant]. This may explain why misuse of quetiapine and other antihistamines have largely been reported in people with a previous history of substance abuse. Substance abuse increases long-term potentiation of the reward system (Saal et al., 2003) and a hyperactive reward system may be necessary for antihistaminic medications to have a reinforcing effect. Behavioral studies in non-human primates have found antihistamines can maintain responses in cocaine-conditioned animals ([Bergman and Spealman, 1986] and [Sannerud et al., 1995]) and lead to motor excitation (Evans and Johanson, 1989). In contrast, the effect of antihistamines in humans is calming or sedating. The difference of effect between non-human primates and humans may indicate divergent reinforcing mechanisms and perhaps a limited relevance of animal models.

(the prospect of an evolutionary adaptation is especially seductive; I'm not sure it should be abandoned so readily)

Fischer cont. said:
Quetiapine has a high antagonistic affinity for the histamine H1 receptor; especially in relationship to its antagonistic affinity for the D2 receptor . . . Other antipsychotics (e.g. clozapine, olanzapine, and chlorpromazine) also have antihistaminic effects, but have not been linked to have high abuse potential. Why would quetiapine have a higher abuse potential than other antihistaminic antipsychotics? One answer is the superior safety profile of quetiapine for side effects, especially movement disorders (Farah, 2005). The rarity of dystonia and extrapyramidal side effects may make quetiapine a more attractive option for misuse compared to other antipsychotics. Quetiapine has a low affinity for and quickly dissociates from dopamine receptors ([Kapur and Seeman, 2000] and [Tauscher et al., 2004]). Dopamine is another important molecule in reward circuitry. High dopamine D2 receptor antagonism in humans is correlated with antipsychotic-induced dysphoria (Mizrahi et al., 2007) and rodent data shows dopamine D1 antagonism abolishes the antihistaminic potentiation of other substances of abuse ([Suzuki et al., 1990] and [Suzuki et al., 1991]). Quetiapine, due to its low affinity and fast disassociation from both D1 and D2 receptors ([Kapur and Seeman, 2000] and [Tauscher et al., 2004]), may have less potential to disrupt any reinforcing antihistaminic effects.

A puzzle piece is missing here. What is unique to quetiapine among antipsychotics is its kinetics at H1 versus D2 (mathematically a partial second derivative, so that even gradual rate differences can have profound differences in the overall effect). The observation that humans seem to be in the process of developing an adaptation to histamine antagonists is compelling. Might we be reacting against a vestigial phenotype when (drug users) express puzzlement and disdain against people who like to put Seroquel up their noses?
 
I guess it depends on what you consider recreational. There is a list of drugs, that if offered, I may consider getting, depending on what I need.

Seroquel is "recreational" or "abused" by myself only in the sense that if I need to pass out hard, I'd take it.

Last time I had it I got really hungry, and attempted to as quickly as possible make a sandwhich, get upstaris to my room, eat it, and pass out. Yea, I failed.

Then one night I took it with Kpins and Vodka, another fail.

Only good property, again, going to sleep
 
The urge to go into HELLO MCFLY mode is strong here. We give pharmacologically-sound reasons for why a quetiapine abuser cannot possibly be enjoying himself, because the substance precludes enjoyment altogether.

Well sure, but It's not like I wrote off the phenomenon altogether. See:

It's a relatively low-affinity dopamine antagonist with proportionally higher affinity for the H1 receptor than others

But either way, I'm still not really sure what relevance dopamine efflux/binding might have to an imprisoned junkie. In more histamine-selective doses, the drug would be far more sedating than anguish-inducing, and likely to attract abuse by bored, impressionable inmates. Further mechanistic speculation seems more than a bit ridiculous when William Occam's methods dictate otherwise. I also can't agree with Fischer. Last I checked, the benzodiazepines are relatively devoid of significant striatal dopaminergic effects, yet stand out as widely abused drugs nonetheless. And I think everyone here knows that the experience of pleasure isn't 100% dependent upon extracellular dopamine levels in the midbrain.

But for the fuck of it...more on the antihistaminic dopamine disinhibition thing:

Dopaminergic effects of histamine administration in the nucleus accumbens and the impact of H1-receptor blockade.

Galosi R, Lenard L, Knoche A, Haas H, Huston JP, Schwarting RK.

Institute of Physiology and Neurophysiology Research Group of Hungarian Academy of Sciences, Pecs University Medical School, Pecs, Hungary.
Abstract

The mesolimbic dopamine system is thought to play a critical role in reward-related processes. A number of studies have shown that lesion or inhibition of histaminergic neurons acting through H1 receptors can potentiate the effects of drug-induced reward (e.g., psychostimulants and opioids) and can enhance the reinforcing effects of electrical stimulation of the brain. Since dopamine transmission in the nucleus accumbens is thought to provide a crucial link in these histaminergic actions, we examined the effects of local histamine application (0.1, 1.0 and 10.0 micromol/l) on dopamine and its metabolites in the nucleus accumbens of anesthetized rats by means of unilateral reverse dialysis. To study the influence of H1 receptors, we also applied the H1-receptor antagonist pyrilamine (10.0 and 20.0 mg/kg, intraperitoneally) 20 min before histamine administration (1 mmol/l). Finally, pyrilamine (0.1, 1.0 and 10.0 micromol/l) was locally administered into the nucleus accumbens. The data show that histamine can enhance extracellular dopamine levels in the nucleus accumbens in a dose-dependent way. This increase was partially antagonized by prior peripheral administration of 10 mg/kg, and was completely blocked by 20 mg/kg, of pyrilamine. Finally, intra-accumbens administration of pyrilamine locally decreased dopamine and increased dihydroxyphenylacetic acid and homovanillic acid levels. These data are discussed with respect to the possible interactions between dopaminergic and histaminergic mechanisms in the mesolimbic system and their relation to mechanisms of reinforcement.

Increased levels of extracellular dopamine in neostriatum and nucleus accumbens after histamine H1 receptor blockade.

Dringenberg HC, de Souza-Silva MA, Schwarting RK, Huston JP.

Department of Psychology, Queen's University, Kingston, Ontario, Canada.
Abstract

The dopaminergic system plays a central role in the processing of reward or reinforcement since drugs that have reinforcing properties all share the ability to elevate dopamine (DA) levels in the nucleus accumbens or neostriatum. Histamine H1 receptor antagonists are known to have reinforcing effects in humans and laboratory rats. Here, we examined the effect of systemic (i.p.) treatment with two H1 antagonists, chlorpheniramine and pyrilamine, on the extracellular levels of DA and its metabolites dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) in the neostriatum and nucleus accumbens of urethane-anesthetized rats. Dopamine and metabolites were measured using in vivo microdialysis and HPLC with electrochemical detection. Saline injections did not produce significant effects on DA, DOPAC, or HVA levels in the neostriatum or nucleus accumbens. In the neostriatum, chlorpheniramine administration (5 and 20 mg/kg) produced a sustained increase in DA to approximately 140 and 180% of pre-injection baseline levels, respectively. In the nucleus accumbens, chlorpheniramine (20 mg/kg) produced a transient increase in DA levels to about 300% of baseline. In both the neostriatum and nucleus accumbens, DOPAC and HVA decreased after chlorpheniramine treatment. Pyrilamine administration (10 and 20 mg/kg) produced a sustained increase in neostriatal DA levels to 140 and 165%, respectively, and accumbens DA increased transiently to 230% after a dose of 20 mg/kg. Levels of neostriatal and accumbens DOPAC and HVA decreased after pyrilamine treatment. These results show that H1 antagonists can potently enhance DA levels in the neostriatum and nucleus accumbens of urethane-anesthetized rats. The neurochemical effects on DA and its metabolites seen here (increased DA, decreased DOPAC and HVA) are similar to those commonly observed with drugs of abuse (e.g. psychostimulants). The interaction of H1 antagonists with dopaminergic transmission may explain the reinforcing effects and abuse potential associated with these compounds.

It's pretty funny that this topic should show up now. It was actually just a couple weeks ago that I was looking into histamine's regulatory influence on the dopamine system and its relevance to antipsychotic drug efficacy. I was pretty surprised at what I found.

Though I suppose the real takeaway is this - quetiapine might have roughly equivalent [likely far less] abuse potential than Benadryl or high-dose Zyrtec with an unreasonable slew of dose-dependent side effects, and is unlikely to garner repeated administration in any poly-drug abuser with ready access to far more forgiving compounds (read: fucking OTC allergy medicine). This is pretty underwhelming stuff.
 
used to be on 500 mg a day dosage in my unstable days. i would in no way remotely compare it to cocaine. i compare it to being a zombie. you feel kinda out of it, i would do what i called "skipping or resetting". i would all of a sudden black out for a split second, like my mind would "blink". it lasts for maybe a second but when you come back you have to gather yourself and think of what was going on (like a cd skipping). was very frustrating after awhile which is why i quit taking it.
 
This drug induces a very unpleasant delirium.

thank god someone said it--i have taken one half-pill of this drug one time (per prescription) and i will never, ever, ever allow that stuff into my body again.

and i've been known to allow stuff into my body that other people find overwhelming.
 
*Shudder* Why would anyone want to even take these, much less snorth them?! I hate these so much. I have a whole bunch of them and will never take them, ever. Why would these act like cocaine? My Dr. LOVES prescribin
 
You really want an answer?

Because it knocks you out. Because there are a lot of people out there who have a really deep, uncontrollable desire to shut down all mental activity, to not having to think and to fear and to suffer for just a few hours. and it's obviously better than drinking, benzos or other addictive and hangover inducing substances.
Besides,
- you can use it to come down from stims
- if you're psychotic (and quite a few addicts and homeless people are) it's self medication

Whats so sick about trying to sleep during boring or hurting periods of your life? And for some people that what most of their life is about.

People do not compulsively use substances because they are *fun*.
 
Yeah.. And occasional extremely intense brainshocks and i even saw a spider appear once in my bed.
This stuff is terrible.

Oh man I took 4mg lorazepam and 1200mg seroquel once (years years back, i saw that same fucking spider, it was white and glowing kinda stenciled

Mother fucker was HUGE crawlin around all over the place
i didn't know what to do
 
I'd say with Seroquel (Quetiapine) the point is VERY simple.

Unlike ALL other Atypical Antipsychotics is has a VERY HIGH H1 antagonism activity.

Prisoners are abusing it? Makes sense, hell a high dose of diphenhydramine I say I would swap a cigarette or whatever happens these days just to temporarily BLOCK the daily depressing life of being in prison out for a bit and get knocked out for sleep.

+ that and the whole "I am drunk, tripping over things, bumping in to walls", "this is kinda like alcohol dude".."oh and the next day the wardens are out trying to kill me **undiagnosed schizophrenic paranoia**" ...EFECT:\

oh and isn't there that song by lil wyte - oxycotton. "...some people melt them down in a needle (oxycontin) and shoot em up, but I pop em with seroquel like glue, see I'm a pill poppa...etc etc". Can imagine a small dose might somehow synergise with oxycodone? ala promethazine (which has 1/10 potency of chlorpromazine), cyclizine with opioids which are known to synergise well.
 
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Quetiapine has very low bioavailability. When snorted, a much larger amount of the drug gets into the blood stream than when taken orally. It is not subjectively euphoric, but is fast acting and very sedating. Nothing like cocaine though.
 
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