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Hallucinogens are active substances that alter consciousness and affect the human psyche. Until now, we know relatively little about their mechanism of action in the brain. Despite their high degree of safety and lack of dependence liability (O’Brien 2001), hallucinogens have been labeled as the most dangerous drugs that exist, being placed into Schedule I of the Controlled Substances Act (CSA). Since September 29, 2004, 5-MeO-DIPT has been permanently controlled as a schedule I substance under the CSA (69 FR 58050) (DEA 2013), because it is used as a substitute for MDMA.

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4. 5-Methoxy-N,N-dimethyltryptamine (5-MeO-DMT) belongs to a group of naturally-occurring psychoactive indolealkylamine drugs. It acts as a nonselective serotonin (5-HT) agonist and causes many physiological and behavioral changes. 5-MeO-DMT is O-demethylated by polymorphic cytochrome P450 2D6 (CYP2D6.
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6. It is an alkaloid, probably derived from L-tryptophan, that has been found in the bark, shoots and leaves of several plant species, including Virola, Acacia, Mimosa and Desmanthus often together with the related compounds N,N-dimethyltryptamine (DMT) and 5-methoxy-N,N-dimethyltryptamine (5-MeO-DMT).

Classical hallucinogens may be divided into two broad categories: tryptamines, e.g., psilocybin, and phenethylamines, e.g., mescaline. Tryptamines comprise two groups of substances: simple tryptamines, such as DMT, 5-MeO-DMT, and ergolines, i.e., their relatively rigid analogues, such as LSD. Based on pharmacological, electrophysiological, and behavioral studies, it is hypothesized that classical hallucinogens produce their effects in animals and probably in humans primarily at cortical 5-HT2A receptor subtype (Aghajanian and Marek 1997, 1999; Glennon et al. 1984; Nelson et al. 1999; Nichols 1997; Scruggs et al. 2003; Smith et al. 1998, 1999; Sipes and Geyer. 1995). The activity of tryptamine hallucinogens was evidenced in drug discrimination studies conducted on rats. It was shown that 5-HT₂ antagonists, like ketanserin and pirenperone blocked the discriminative stimulus effects of phenethylamine and tryptamine hallucinogens (Colpaert and Janssen 1983; Leysen et al. 1982). In addition, the head-twitch response (HTR) test is another animal model widely used to reliably distinguish hallucinogenic and nonhallucinogenic drugs the action of which is mediated by agonists of 5-HT2A receptors in mice and rats (González-Maeso et al. 2007). Schreiber et al. (1995) showed that head twitches induced by the phenylethylamine hallucinogen (±)DOI were abolished by low doses of the 5-HT2A-selective antagonist M100907, but not by the selective 5-HT2C antagonist, SB 200,646A. Mediation of behavioral effects induced by hallucinogens via 5-HT2A receptor is supported by electrophysiological and biochemical findings. Electrophysiological data demonstrated that stimulation of postsynaptic 5-HT2A receptors on pyramidal cells by hallucinogens led to glutamate-dependent increase in the activity of pyramidal neurons in layer V of the prefrontal cortex (Aghajanian and Marek 1997, 1999; Beique et al. 2007; Puig et al. 2003), while microdialysis studies showed enhancement of glutamate release by selective 5-HT2A agonist (±)DOI and LSD (Muschamp et al. 2004; Scruggs et al. 2003). Hallucinogens by acting at 5-HT2A receptors in the VTA may also activate brain DA pathways directly via somatodendritic receptors or presynaptic receptors in mesolimbic or mesocortical DA terminals. They may also affect DA pathways indirectly by modulating the GABA-ergic interneurons in the VTA (Celada et al. 2001; Vazquez-Borsetti et al. 2009). Besides 5-HT2A receptor activity, LSD, and tryptamines but not the phenethylamine-type hallucinogens, have high affinity for 5-HT1A receptors (deMontigny and Aghajanian 1977; Titeler et al. 1988). Administration of LSD, psilocybin, DMT, and 5-MeO-DMT caused a reduction in the firing rate of cells in the dorsal raphe nucleus (deMontigny and Aghajanian 1977). This observation led to the hypothesis that inhibition of 5-HT neuron activity via 5-HT1A autoreceptors might be the underlying mechanism for hallucinogenesis. However, 5-HT1A receptors, besides somatodendritic location, have a high postsynaptic density in limbic and cortical brain regions (Hamon et al. 1990; Pazos and Palacios 1985); and their stimulation leads to neuronal hyperpolarization (Hamon et al. 1990). In addition, it has been shown recently that 5-HT1A receptors are co-localized with 5-HT2A receptors on cortical pyramidal cells (Martin-Ruiz et al. 2001), where the two receptor types have opposing effects (Araneda and Andrade 1991). Willins and Meltzer (1997) reported that the 5-HT1A agonist 8-OH-DPAT inhibited (±)DOI-induced head twitches in rats. It was concluded that the activation of 5-HT1A receptors inhibited functional effects mediated by 5-HT2A receptors. Furthermore, most of the potent hallucinogenic compounds are also agonists of the 5-HT2C receptor (Chambers et al. 2001). Serotonin 5-HT2A and 5-HT2C receptors are both present on cortical GABA-ergic interneurons (Santana et al. 2004) and their activation has been observed to produce opposing behavioral effects (Fantegrossi et al. 2010). Moreover, the 5-HT2C receptors found in the VTA and nucleus accumbens exert tonic inhibitory action on mesolimbic and mesocortical dopaminergic neurons, and stimulation of those receptors suppresses DA release in the cortex and nucleus accumbens (De Deurwaerdere et al. 2004; Di Matteo et al. 1999). Thus, 5-HT2C receptors may play a modulatory role upon the control of dopaminergic-serotonergic-glutamatergic interactions in the mechanism of action of hallucinogens.

5-Methoxy-N,N-diisopropyltryptamine (5-MeO-DIPT), belonging to the tryptamine class of hallucinogens, in contrast to naturally occurring 5-MeO-DMT, DMT, or bufotenine, is a synthetic designer drug synthesized by Shulgin (1980). 5-MeO-DIPT, a popular illicit drug with a street name “foxy” or “foxy methoxy” is taken alone or mixed with other stimulants, e.g., with MDMA as ecstasy tablets (DEA 2013). It has been demonstrated that 5-MeO-DIPT is a competitive serotonin transporter (SERT) inhibitor and has a lower affinity for dopamine transporter (DAT) (Nagai et al. 2007; Sogawa et al. 2007). Fantegrossi et al. (2006) reported that hallucinogenic activity of 5-MeO-DIPT in mice was caused by the stimulation of postsynaptic 5-HT2A receptors, but 5-MeO-DIPT had also high affinity for 5-HT1A or 5-HT2C receptors as shown in vitro by Blough et al. (2014). 5-MeO-DIPT induced head-twitch responses in the mouse, and this effect was antagonized by the selective 5-HT2A receptor antagonist M100907 (Fantegrossi et al. 2006). Sogawa et al. (2007) demonstrated a marked cytotoxicity of 5-MeO-DIPT at high concentrations, as assessed by a cell viability assay in COS-7 cells. In another in vitro study, sustained exposure to 5-MeO-DIPT markedly decreased the intracellular 5-HT content in the mesencephalic slice culture (Nakagawa and Kaneko 2008). Clinical data indicated potent multi-organ effects of 5-MeO-DIPT as the users experienced euphoria, disinhibition, increased sociability, visual, and auditory hallucinations, but also effects like mioclonus, restlessness, insomnia and anxiety, nausea, vomiting, and diarrhea (Tittarelli et al. 2015). The possible toxicity of 5-MeO-DIPT is suggested by cognitive deficits observed in animals in some behavioral tests. It was found that 5-MeO-DIPT injected repeatedly to adolescent rats showed deleterious effects on learning and memory in adulthood (Compton et al. 2011; Skelton et al. 2009). Repeated doses of 5-MeO-DIPT altered ability of rats to perform certain cognitive tasks and caused hypoactivity and minor changes in 5-HT turnover in several brain regions (Williams et al. 2007).

Knowing the risk associated with 5-MeO-DIPT used recreationally and scarcity of in vivo data on the mechanism of its action in the brain, we examined the effects of 5-MeO-DIPT on neurotransmitter levels in several brain regions, and subsequent possible oxidative DNA damage. We also tried to show the 5-HT2A and 5-HT1A receptor effects of 5-MeO-DIPT in behavioral tests. Since the head-twitch response (HTR) is a behavior that is mediated by agonistic action at 5-HT2A receptors (González-Maeso et al. 2007), we tested the changes induced by several doses of 5-MeO-DIPT in the head-twitch response in comparison to the selective phenylethylamine 5-HT2A receptor agonist (±)DOI. Since binding data showed high affinity of 5-MeO-DIPT for 5-HT1A receptor, we also investigated 5-MeO-DIPT in vivo activity by using forepaw treading as the syndrome induced by 8-OH-DPAT and mediated via this receptor (Smith and Peroutka 1986).

O-Acetylpsilocin (also known as psilocetin, 4-acetoxy-DMT, or 4-AcO-DMT) is a semi-synthetic psychoactive drug and has been suggested by David Nichols to be a potentially useful alternative to psilocybin for pharmacological studies, as they are both believed to be prodrugs of psilocin.^[2] However, some users report that O-acetylpsilocin's subjective effects differ from that of psilocybin and psilocin.^[3] It is the acetylated form of the psilocybin mushroomalkaloidpsilocin and is a lower homolog of 4-AcO-MET, 4-AcO-DET, 4-AcO-MiPT and 4-AcO-DiPT.

• 4Legality

History[edit]

O-Acetylpsilocin (psilocetin) and several other esters of psilocin were patented on January 16, 1963 by Sandoz Ltd. via Albert Hofmann & Franz Troxler.^[1][4] Despite this, psilocetin remains a psychedelic compound with a limited history of use. It is theorized to be a prodrug for psilocin, as is psilocybin, which occurs naturally in most species of hallucinogenic mushrooms. This is because the aromatic acetyl moiety on the 4th position is subject to deacetylation by acidic conditions such as those found in the stomach.^[5] Psilocetin is O-acetylated psilocin, whereas psilocybin is O-phosphorylated.

Chemistry[edit]

O-Acetylpsilocin can be obtained by acetylation of psilocin under alkaline or strongly acidic conditions. It is, therefore, a semi-synthetic compound. It is believed to be a prodrug of psilocin, however, speculation that psilocetin may itself also be active exists. O-Acetylpsilocin is more resistant than psilocin to oxidation under basic conditions due to its acetoxy group. While O-acetylpsilocin is not well researched (sometimes viewed negatively as a research chemical, as opposed to psilocin and psilocybin), though it is not as difficult to produce as psilocybin. Due to their similar mechanism of action, this may further support ideas of O-acetylpsilocin possibly serving as an appropriate substitute to psilocybin for use in research of the effects psychedelic compounds in medicine.^[2]

Pharmacology[edit]

See psilocin for more details.

In the body O-acetylpsilocin is deacetylated to psilocin by deacetylases/acetyltransferases during first pass metabolism^{[citation needed]} and during subsequent passes through the liver (evident as psilacetin is also active via parenteral routes of ingestion).

Claims of subjective differences in effect between the acetylated and non-acetylated forms of psilocin differ:^[3] some users report that O-acetylpsilocin lasts slightly longer while others report that it lasts for a considerably shorter time. Many users report less body load and nausea compared to psilocin. Some users find that the visual distortions produced by O-acetylpsilocin more closely resemble those produced by DMT than those produced by psilocin. These differences could be possible if psilocetin is active itself and not merely as a prodrug. Despite this, there have been no controlled clinical studies to distinguish any effects of psilocetin, psilocin, and psilocybin from one another.

Legality[edit]

Australia[edit]

O-Acetylpsilocin can be considered an analog of psilocin making it a schedule 9 prohibited substance in Australia under the Poisons Standard (October 2015).^[6] A Schedule 9 substance is a substance which may be abused or misused, the manufacture, possession, sale or use of which should be prohibited by law except when required for medical or scientific research, or for analytical, teaching or training purposes with approval of Commonwealth and/or State or Territory Health Authorities.^[6]

United States[edit]

O-Acetylpsilocin is ambiguously legal for use as a lab reagent or research chemical; however, it is an acetate ester of psilocin, meaning it would be considered Schedule I under the Federal Analogue Act if sold for human consumption.

United Kingdom[edit]

O-Acetylpsilocin, being an ester of psilocin, is a class A drug in the UK under the Misuse of Drugs Act 1971.^[7]

Italy[edit]

O-Acetylpsilocin is illegal in Italy as it is an ester of a prohibited substance.

Sweden[edit]

The Riksdag added 4-AcO-DMT to Narcotic Drugs Punishments Act under swedish schedule I ('substances, plant materials and fungi which normally do not have medical use' ) as of January 25, 2017, published by Medical Products Agency (MPA) in regulation HSLF-FS 2017:1 listed as 4-acetoxi-N,N-dimetyltryptamin.^[8]

See also[edit]

References[edit]

1. ^ ^abUS patent 3075992, Hofmann A, Troxler F, 'Esters of indoles', assigned to Sandoz Ltd.
2. ^ ^abNichols D, Fescas S (1999). 'Improvements to the Synthesis of Psilocybin and a Facile Method for Preparing the O-Acetyl Prodrug of Psilocin'(PDF). Synthesis. 1999 (6): 935–938. CiteSeerX10.1.1.690.8071. doi:10.1055/s-1999-3490. Archived(PDF) from the original on 17 February 2012. Retrieved 17 January 2012.
3. ^ ^ab'4-AcO-DMT (also 4-acetoxy-N,N-dimethyltryptamine) : Erowid Exp: Main Index'. www.erowid.org. Archived from the original on 2010-07-28.
4. ^US 3075992
5. ^Staněk J, Černá MJ (January 1963). 'Acidic deacetylation of sugar acetates'. Tetrahedron Letters. 4 (1): 35–7. doi:10.1016/S0040-4039(01)90572-6.
6. ^ ^ab'Poisons Standard October 2015'. Federal Register of Legislation. Australian Government. Archived from the original on 2016-01-19. Retrieved 2016-01-06.
7. ^'Misuse of Drugs Act 1971'. Schedule 2 Part I,Actof1971.
8. ^'Archived copy'(PDF). Archived(PDF) from the original on 2017-10-31. Retrieved 2017-04-21.CS1 maint: Archived copy as title (link)

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External links[edit]

• 'Esters of Indoles' US Patent # 3,075,992 - Awarded to Sandoz Ltd. (via Albert Hofmann & Franz Troxler) on January 29, 1963.

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