Mirtazapine. Mirtazapine (brand names: Avanza, Axit, Mirtaz, Mirtazon, Remeron, Zispin)[6] is a noradrenergic and specific serotonergic antidepressant (NaSSA) introduced by Organon International in the United States in 1996,[2] and is used primarily in the treatment of depression. It is also commonly used as an anxiolytic, hypnotic, antiemetic, and appetite stimulant. In structure, mirtazapine can also be classified as a tetracyclic antidepressant (TeCA) and is the 6-aza analogue of mianserin.[6] It is also racemic - occurs as a combination of both R and S-stereoisomers.[6] Its patent expired in 2004, so generic versions are available.[7] §Medical uses[edit] §Approved and off-label[edit] Mirtazapine's primary use is the treatment of major depressive disorder and other mood disorders.[8][9] However, it has also been found useful in alleviating the following conditions and may be prescribed off-label for their treatment: §Investigational[edit] §Feline[edit] §Efficacy and tolerability[edit] §[edit] Headache.
5-MeO-DMT. 5-MeO-DMT (5-methoxy-N,N-dimethyltryptamine) is a powerful psychedelic tryptamine. It is found in a wide variety of plant and psychoactive toad species and, like its close relatives DMT and bufotenin (5-HO-DMT), it has been used as an entheogen by South American shamans for thousands of years. [citation needed] Chemistry[edit] History[edit] Traditionally 5-MeO-DMT has been used in psychedelic snuff made from virola bark resin, and may be a trace constituent of ayahuasca when plants such as Diplopterys cabrerana are used as an admixture. 5-MeO-DMT is also found in the venom of the Colorado River toad (Bufo alvarius), although there is no direct evidence this was used as a hallucinogen until recent times. Religious use[edit] 5-MeO-DMT is a sacrament of the Church of the Tree of Life. Pharmacology[edit] Use and effects[edit] Although similar in many respects to its close relatives DMT and bufotenin (5-OH-DMT), the effects are typically not as visual.
Positive[edit] Neutral[edit] Negative[edit] S. Phenelzine. Atropine. In general, atropine counters the "rest and digest" activity of glands regulated by the parasympathetic nervous system. This occurs because atropine is a competitive antagonist of the muscarinic acetylcholine receptors (acetylcholine being the main neurotransmitter used by the parasympathetic nervous system). Atropine dilates the pupils, increases heart rate, and reduces salivation and other secretions. Atropine is a core medicine in the World Health Organization's "Essential Drugs List", which is a list of minimum medical needs for a basic health care system.[1] Name[edit] The species name "belladonna" ("beautiful woman" in Italian) comes from the original use of deadly nightshade to dilate the pupils of the eyes for cosmetic effect.
Both atropine and the genus name for deadly nightshade derive from Atropos, one of the three Fates who, according to Greek mythology, chose how a person was to die. Medical uses[edit] Ophthalmic use[edit] Optical penalization[edit] Resuscitation[edit] Voacangine. Voacangine (12-methoxyibogamine-18-carboxylic acid methyl ester) is an alkaloid found predominantly in the rootbark of the Voacanga africana tree, as well as in other plants such as Tabernanthe iboga, Tabernaemontana africana, Trachelospermum jasminoides and Ervatamia yunnanensis.[2][3][4][5] It is an iboga alkaloid which commonly serves as a precursor for the semi-synthesis of ibogaine.[6] It has also been demonstrated in animals to have similar anti-addictive properties to ibogaine itself.[7] See also[edit] References[edit] Jump up ^ "Compound Report Card CHEMBL182120 - Voacangine".
ChEMBL. Harmaline. Harmaline is a fluorescent psychoactive indole alkaloid from the group of harmala alkaloids and beta-carbolines. It is the reduced hydrogenated form of harmine. Occurrence in nature[edit] Various plants contain harmaline including Peganum harmala (Syrian Rue) as well as the hallucinogenic drink ayahuasca, which is traditionally brewed using Banisteriopsis caapi.
Present at 3% by dry weight, the harmala alkaloids may be extracted from the Syrian Rue seeds.[1] Effects[edit] Harmaline is a central nervous system stimulant and a "reversible inhibitor of MAO-A (RIMA)".[2] This means that the risk of a hypertensive crisis, a dangerous high blood pressure crisis from eating tyramine-rich foods such as cheese, is likely lower with harmaline than with irreversible MAOIs such as phenelzine. United States Patent Number 5591738 describes a method for treating various chemical dependencies via the administration of harmaline and or other beta-carbolines.[6] See also[edit] References[edit] Harmine. Harmine is a fluorescent harmala alkaloid belonging to the beta-carboline family of compounds. It occurs in a number of different plants, most notably the Middle Eastern plant harmal or Syrian rue (Peganum harmala) and the South American vine Banisteriopsis caapi (also known as "yage" or "ayahuasca").
Harmine reversibly inhibits monoamine oxidase A (MAO-A), an enzyme which breaks down monoamines, making it a RIMA. Harmine selectively binds to MAO-A but does not inhibit the variant MAO-B.[5] Uses[edit] Monoamines include neurotransmitters (serotonin, dopamine), hormones (melatonin, epinephrine, norepinephrine) and psychedelic drugs (psilocybin, DMT and mescaline). P. harmala and B. caapi are both traditionally used for their psychoactive effects. Harmine is also a useful fluorescent pH indicator. With the radioisotope carbon-11 harmine is used in positron emission tomography neuroimaging to examine its binding to MAO-A.[6] Anticancer[edit] Adverse effects[edit] Overdosage[edit] See also[edit] Tranylcypromine. Tranylcypromine (Parnate, Jatrosom) is a drug of the substituted phenethylamine and amphetamine classes which acts as a monoamine oxidase inhibitor (MAOI)—it is a nonselective and irreversible inhibitor of the enzyme monoamine oxidase (MAO).[1][2] It is used as an antidepressant and anxiolytic agent in the clinical treatment of mood and anxiety disorders, respectively.
History[edit] The drug was introduced by Smith, Kline and French in the United Kingdom in 1960, and approved in the United States in 1961.[5] It was withdrawn from the market in February 1964 due to a number of patient deaths involving hypertensive crises with intracranial bleeding. However, it was reintroduced later that year with more limited indications and specific warnings of the risks.[6] Clinical use[edit] Effectiveness[edit] Contraindications[edit] Therapeutic contraindications of tranylcypromine include: Dietary restrictions[edit] Adverse effects[edit] At least one case of the abuse of tranylcypromine has been noted. Harmala alkaloid. Pinoline. Pinoline is a methoxylated tryptoline (5-methoxytryptoline) that is produced in the pineal gland during the metabolism of melatonin. Its IUPAC name is 6-methoxy-1,2,3,4-tetrahydro-β-carboline, usually abbreviated as 6-MeO-THBC, and its more common name is a combination of "pineal beta-carboline".[1] The biological activity of this molecule is of interest as a potential free radical scavenger, also known as an antioxidant,[2] and as a monoamine oxidase A inhibitor.[3] Bausch & Lomb filed a patent for this molecule as a potential drug delivery device to treat various ophthalmic disorders in 2006.[4] Protection of cellular membranes[edit] Aluminium toxicity causes an increase in lipid peroxidation, with most damage occurring in the brain.
A recent review of studies shows pinoline and melatonin to be effective at reducing the lipid peroxidation. Studies included both human and animal subjects. The studies’ results support that pinoline has antioxidant properties.[5] References[edit] Dimethyltryptamine. History[edit] Another historical milestone is the discovery of DMT in plants frequently used by Amazonian natives as additive to the vine Banisteriopsis caapi to make ayahuasca decoctions.
Biosynthesis[edit] Biosynthetic pathway for N,N-dimethyltryptamine This transmethylation mechanism has been repeatedly and consistently proven by radiolabeling of SAM methyl group with carbon-14 (14C-CH3)SAM).[22][20][24][25][26] Evidence in mammals[edit] In 2013, researchers first reported DMT in the pineal gland microdialysate of rodents.[28] A study published in 2014 reported the biosynthesis of N,N-dimethyltryptamine (DMT) in the human melanoma cell line SK-Mel-147 including details on its metabolism by peroxidases. [29] In a 2014 paper, a group first demonstrated the immunomodulatory potential of DMT and 5-MeO-DMT through the Sigma-1_receptor of human immune cells. INMT[edit] Endogenous DMT[edit] The first claimed detection of mammalian endogenous DMT was published in June 1965: German researchers F.
Diethyltryptamine. Chemistry[edit] DET is an analogue of the common tryptamine hallucinogen N,N-Dimethyltryptamine or DMT. Pharmacology[edit] The mechanism of action is thought to be serotonin receptor agonism, much like other classic psychedelics.[2] DET is sometimes preferred over DMT because it can be taken orally whereas DMT cannot. Biochemistry[edit] Though DET is a synthetic compound with no known natural sources it has been used with mycelium of Psilocybe cubensis to produce the synthetic chemicals 4-PO-DET (Ethocybin) and 4-HO-DET (Ethocin), as opposed to the naturally occurring 4-PO-DMT (Psilocybin) and 4-HO-DMT (Psilocin). Psychosis model[edit] See also[edit] References[edit] External links[edit] Psilocin. Psilocin (also known as 4-OH-DMT, psilocine, psilocyn, or psilotsin), is a substituted tryptamine alkaloid and a serotonergic psychedelic substance. It is present in most psychedelic mushrooms together with its phosphorylated counterpart psilocybin.
Psilocin is a Schedule I drug under the Convention on Psychotropic Substances.[2] The mind-altering effects of psilocin are highly variable and subjective and resemble those of LSD and DMT. Chemistry[edit] Psilocin and its phosphorylated cousin, psilocybin, were first isolated and named in 1958 by Swiss chemist Albert Hofmann. Hofmann obtained the chemicals from laboratory-grown specimens of the entheogenic mushroom Psilocybe mexicana. Psilocin is relatively unstable in solution due to its phenolic hydroxy (-OH) group. Structural analogs[edit] Pharmacology[edit] Psilocin is the pharmacologically active agent in the body after ingestion of psilocybin or some species of psychedelic mushrooms. Psilocin's half-life ranges from 1 to 3 hours.[1] Baeocystin. Baeocystin was first isolated from the mushroom Psilocybe baeocystis,[1] and later from P. semilanceata,[2] Panaeolus renenosus, Panaeolus subbalteatus, and Copelandia chlorocystis.[3] It was first synthesized by Troxler et al. (1959).[4] Little information exists with regard to human pharmacology, but in the book Magic Mushrooms Around the World, author Jochen Gartz reports being aware of a study in which "10 mg of baeocystin were found to be about as psychoactive as a similar amount of psilocybin.
"[citation needed] Gartz also reported in a research paper that a self-administered assay of 4 mg of baeocystin caused "a gentle hallucinogenic experience".[5] Muscimol. Muscimol (agarin, pantherine) is the major psychoactive alkaloid present in many mushrooms of the Amanita genus. Muscimol is a potent, selective agonist for the GABAA receptors and displays sedative-hypnotic effects. Chemistry[edit] Muscimol is the psychoactive compound responsible for the effects of Amanita muscaria intoxication. Ibotenic acid, a neurotoxic secondary metabolite of Amanita muscaria, serves as a prodrug to muscimol when the mushroom is ingested or dried, converting to muscimol via decarboxylation. Biology[edit] Pharmacology[edit] While muscimol is conventionally thought of as a selective GABAA agonist, it is also a partial agonist at the GABAA-rho receptor, and so its range of effects results from a combined action at both targets.[7] In patients with Huntington's disease and chronic schizophrenia, oral doses of muscimol have been found to cause a rise of both prolactin and growth hormone.[8] Toxicity[edit] Effects[edit] See also[edit] Notes[edit] References[edit]
Indole alkaloid. History[edit] The action of some indole alkaloids has been known for ages. Aztecs used the psilocybin mushrooms which contain alkaloids psilocybin and psilocin. The flowering plant Rauwolfia serpentina which contains reserpine was a common medicine in India around 1000 BC. Africans used the roots of the perennial rainforest shrub Iboga, which contain ibogaine, as a stimulant. An infusion of Calabar bean seeds was given to people accused of crime in Nigeria: its rejection by stomach was regarded as a sign of innocence, otherwise, the person was killed via the action of physostigmine, which is present in the plant and which causes paralysis of the heart and lungs.[3] Consumption of rye and related cereals contaminated with the fungus Claviceps purpurea causes ergot poisoning and ergotism in humans and other mammals.
The first indole alkaloid, strychnine, was isolated by Pierre Joseph Pelletier and Joseph Bienaimé Caventou in 1818 from the plants of the Strychnos genus. Classification[edit] Psilocybin. Psilocybin[nb 1] (/ˌsɪləˈsaɪbɪn/ SIL-ə-SY-bin) is a naturally occurring psychedelic compound produced by more than 200 species of mushrooms, collectively known as psilocybin mushrooms.
The most potent are members of the genus Psilocybe, such as P. azurescens, P. semilanceata, and P. cyanescens, but psilocybin has also been isolated from about a dozen other genera. As a prodrug, psilocybin is quickly converted by the body to psilocin, which has mind-altering effects similar (in some aspects) to those of LSD, mescaline, and DMT. In general, the effects include euphoria, visual and mental hallucinations, changes in perception, a distorted sense of time, and spiritual experiences, and can include possible adverse reactions such as nausea and panic attacks. History[edit] Early[edit] Modern[edit] Albert Hofmann (shown here in 1993) purified psilocybin and psilocin from Psilocybe mexicana in the late 1950s. Occurrence[edit] Aporphine. Thujone. Melatonin. Myristicin. Tryptophan. Tryptamine. Theophylline. Methysergide. Too much Ecstasy? The man who took 40,000 MDMA pills in 9 years. MDMA. Nicotine. Caffeine. Lisuride. Arecoline.
Piracetam. Tiagabine. N-Methyltryptamine. Anandamide. Neurotransmitters and Drugs Chart. Ergotamine. Hordenine. Theobromine. Iproniazid. Scopolamine. Tryptoline. Heroin. Morphine. Diphenhydramine. Doxylamine. Bupropion. Methylphenidate. Yuremamine. Bufotenin. Oxycodone. Codeine. Phencyclidine. Amphetamine. Ketamine. MDMA. Cannabinoid. Ethanol. Beta-Carboline. Nuciferine. Indole alkaloid. Tropane alkaloid. Elemicin. Gramine. Cocaine. Online Books : "TIHKAL" - The Continuation" by Alexander and Ann Shulgin. Ergometrine. Ergoline. Lysergic acid hydroxyethylamide. Ergine. Methylergometrine. Lysergic acid diethylamide. Pergolide. Tetrahydrocannabinol. Hyoscyamine.
Mescaline. Salvinorin A. Triterpenoid saponins. Ibogaine.