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Grayanotoxins are a group of toxic [[Diterpene|diterpenes]] found in the ericacaeae family of plants <ref name=":0">Gunduz A, Turedi S, Russell RM, Ayaz FA. Clinical review of grayanotoxin/mad honey poisoning past and present. Clin Toxicol (Phila). 2008 Jun;46(5):437-42. doi: 10.1080/15563650701666306. PMID: 18568799.</ref>. More than 25 grayanotoxin isoforms have been isolated from [[rhododendron]], though grayanotoxin I and grayanotoxin III are considered to be the most responsible for the toxic pharmacological effects of grayanotoxin-containing plants.<ref>Jansen SA, Kleerekooper I, Hofman ZL, Kappen IF, Stary-Weinzinger A, van der Heyden MA. Grayanotoxin poisoning: 'mad honey disease' and beyond. Cardiovasc Toxicol. 2012 Sep;12(3):208-15. doi: 10.1007/s12012-012-9162-2. PMID: 22528814; PMCID: PMC3404272.</ref> Grayanotoxin I, as well as grayanotoxin III, act as [[Agonist|agonists]] of [[Neuron|voltage-gated sodium channels.]]<ref>Yuki T, Yamaoka K, Yakehiro M, Seyama I. State-dependent action of grayanotoxin I on Na(+) channels in frog ventricular myocytes. J Physiol. 2001 Aug 1;534(Pt 3):777-90. doi: 10.1111/j.1469-7793.2001.00777.x. PMID: 11483708; PMCID: PMC2278746.</ref><ref name=":1">Kim SE, Shin MC, Akaike N, Kim CJ. Presynaptic effects of grayanotoxin III on excitatory and inhibitory nerve terminals in rat ventromedial hypothalamic neurons. Neurotoxicology. 2010 Mar;31(2):230-8. doi: 10.1016/j.neuro.2009.12.006. Epub 2009 Dec 28. PMID: 20038438.</ref> Through this mechanism, grayanotoxins increase the release of [[Neurotransmitter|neurotransmitters]] in the central nervous system such as [[GABA]] <ref name=":1" />, [[glutamate]] <ref name=":1" />, and [[acetylcholine]] <ref>Pischon H, Petrick A, Müller M, Köster N, Pietsch J, Mundhenk L. Grayanotoxin I Intoxication in Pet Pigs. ''Veterinary Pathology''. 2018;55(6):896-899. doi:10.1177/0300985818789482</ref>. Additionally, grayanotoxin III may act as an [[antagonist]] of [[Glutamate|central glutamate receptors]], further contributing to [[Depressant|CNS depressant]] effects <ref>Ohgaki T, Uchida S, Meguri H, Ogita K, Yoneda Y. Preventive action of quisqualic acid against grayanotoxin-induced suppression of locomotor activity in mice. Neuropharmacology. 1988 Oct;27(10):1045-53. doi: 10.1016/0028-3908(88)90066-4. PMID: 3070432.</ref>. Reports of grayanotoxin intoxication include symptoms of the [[Cholinergics|cholinergic]] toxidrome such as [[Decreased heart rate|decreased heart rate]], [[Decreased blood pressure|hypotension]], and an [[Cognitive effects|altered mental status]] <ref name=":0" />.
Grayanotoxins are a group of toxic [[Diterpene|diterpenes]] found in the ericacaeae family of plants <ref name=":0">Gunduz A, Turedi S, Russell RM, Ayaz FA. Clinical review of grayanotoxin/mad honey poisoning past and present. Clin Toxicol (Phila). 2008 Jun;46(5):437-42. doi: 10.1080/15563650701666306. PMID: 18568799.</ref>. More than 25 grayanotoxin isoforms have been isolated from [[rhododendron]], though grayanotoxin I and grayanotoxin III are considered to be the most responsible for the toxic pharmacological effects of grayanotoxin-containing plants.<ref>Jansen SA, Kleerekooper I, Hofman ZL, Kappen IF, Stary-Weinzinger A, van der Heyden MA. Grayanotoxin poisoning: 'mad honey disease' and beyond. Cardiovasc Toxicol. 2012 Sep;12(3):208-15. doi: 10.1007/s12012-012-9162-2. PMID: 22528814; PMCID: PMC3404272.</ref> Grayanotoxin I, as well as grayanotoxin III, act as [[Agonist|agonists]] of [[Neuron|voltage-gated sodium channels.]]<ref>Yuki T, Yamaoka K, Yakehiro M, Seyama I. State-dependent action of grayanotoxin I on Na(+) channels in frog ventricular myocytes. J Physiol. 2001 Aug 1;534(Pt 3):777-90. doi: 10.1111/j.1469-7793.2001.00777.x. PMID: 11483708; PMCID: PMC2278746.</ref><ref name=":1">Kim SE, Shin MC, Akaike N, Kim CJ. Presynaptic effects of grayanotoxin III on excitatory and inhibitory nerve terminals in rat ventromedial hypothalamic neurons. Neurotoxicology. 2010 Mar;31(2):230-8. doi: 10.1016/j.neuro.2009.12.006. Epub 2009 Dec 28. PMID: 20038438.</ref> Through this mechanism, grayanotoxins increase the release of [[Neurotransmitter|neurotransmitters]] in the central nervous system such as [[GABA]] <ref name=":1" />, [[glutamate]] <ref name=":1" />, and [[acetylcholine]] <ref>Pischon H, Petrick A, Müller M, Köster N, Pietsch J, Mundhenk L. Grayanotoxin I Intoxication in Pet Pigs. ''Veterinary Pathology''. 2018;55(6):896-899. doi:10.1177/0300985818789482</ref>.
Additionally, grayanotoxin III may act as an [[antagonist]] of [[Glutamate|central glutamate receptors]], further contributing to [[Depressant|CNS depressant]] effects <ref>Ohgaki T, Uchida S, Meguri H, Ogita K, Yoneda Y. Preventive action of quisqualic acid against grayanotoxin-induced suppression of locomotor activity in mice. Neuropharmacology. 1988 Oct;27(10):1045-53. doi: 10.1016/0028-3908(88)90066-4. PMID: 3070432.</ref>. Reports of grayanotoxin intoxication include symptoms of the [[Cholinergics|cholinergic]] toxidrome such as [[Decreased heart rate|decreased heart rate]], [[Decreased blood pressure|hypotension]], and an [[Cognitive effects|altered mental status]] <ref name=":0" />.
==Subjective effects==
==Subjective effects==
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Grayanotoxins are an active constituent of a variety of plants with a history of medicinal and recreational use, including species of rhododendron and monotropa uniflora[1]. Most commonly, grayanotoxins are consumed in the form of mad honey, which is contaminated with grayanotoxins from bees that pollinate rhododendron flowers [2]. Mad honey is reportedly used as an aphrodisiac, painkiller, treatment for hypertension, and as a recreational drug, particularly in Nepal and the Black Sea region of Turkey [2]. Historically, mad honey has been added to alcoholic drinks to increase their potency [3].
Grayanotoxins are a group of toxic diterpenes found in the ericacaeae family of plants [4]. More than 25 grayanotoxin isoforms have been isolated from rhododendron, though grayanotoxin I and grayanotoxin III are considered to be the most responsible for the toxic pharmacological effects of grayanotoxin-containing plants.[5] Grayanotoxin I, as well as grayanotoxin III, act as agonists of voltage-gated sodium channels.[6][7] Through this mechanism, grayanotoxins increase the release of neurotransmitters in the central nervous system such as GABA[7], glutamate[7], and acetylcholine[8].
Disclaimer: The effects listed below cite the Subjective Effect Index (SEI), an open research literature based on anecdotal user reports and the personal analyses of PsychonautWikicontributors. As a result, they should be viewed with a healthy degree of skepticism.
It is also worth noting that these effects will not necessarily occur in a predictable or reliable manner, although higher doses are more liable to induce the full spectrum of effects. Likewise, adverse effects become increasingly likely with higher doses and may include addiction, severe injury, or death ☠.
Physical effects
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As a result, it may contain incomplete or even dangerously wrong information! You can help by expanding upon or correcting it. Note: Always conduct independent research and use harm reduction practices if using this substance.
Warning:Many psychoactive substances that are reasonably safe to use on their own can suddenly become dangerous and even life-threatening when combined with certain other substances. The following list provides some known dangerous interactions (although it is not guaranteed to include all of them).
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↑"Monotropa uniflora Indian Pipe". Plants for a Future. Retrieved 2022-08-13.
↑ 2.02.1Ullah S, Khan SU, Saleh TA, Fahad S. Mad honey: uses, intoxicating/poisoning effects, diagnosis, and treatment. RSC Adv. 2018 May 22;8(33):18635-18646. doi: 10.1039/c8ra01924j. PMID: 35541133; PMCID: PMC9080652
↑"Grayanotoxins". Foodborne Pathogenic Microorganisms and Natural Toxins Handbook. US FDA. 2012. Retrieved August 7, 2015.
↑ 4.04.1Gunduz A, Turedi S, Russell RM, Ayaz FA. Clinical review of grayanotoxin/mad honey poisoning past and present. Clin Toxicol (Phila). 2008 Jun;46(5):437-42. doi: 10.1080/15563650701666306. PMID: 18568799.
↑Jansen SA, Kleerekooper I, Hofman ZL, Kappen IF, Stary-Weinzinger A, van der Heyden MA. Grayanotoxin poisoning: 'mad honey disease' and beyond. Cardiovasc Toxicol. 2012 Sep;12(3):208-15. doi: 10.1007/s12012-012-9162-2. PMID: 22528814; PMCID: PMC3404272.
↑Yuki T, Yamaoka K, Yakehiro M, Seyama I. State-dependent action of grayanotoxin I on Na(+) channels in frog ventricular myocytes. J Physiol. 2001 Aug 1;534(Pt 3):777-90. doi: 10.1111/j.1469-7793.2001.00777.x. PMID: 11483708; PMCID: PMC2278746.
↑ 7.07.17.2Kim SE, Shin MC, Akaike N, Kim CJ. Presynaptic effects of grayanotoxin III on excitatory and inhibitory nerve terminals in rat ventromedial hypothalamic neurons. Neurotoxicology. 2010 Mar;31(2):230-8. doi: 10.1016/j.neuro.2009.12.006. Epub 2009 Dec 28. PMID: 20038438.
↑Pischon H, Petrick A, Müller M, Köster N, Pietsch J, Mundhenk L. Grayanotoxin I Intoxication in Pet Pigs. Veterinary Pathology. 2018;55(6):896-899. doi:10.1177/0300985818789482
↑Ohgaki T, Uchida S, Meguri H, Ogita K, Yoneda Y. Preventive action of quisqualic acid against grayanotoxin-induced suppression of locomotor activity in mice. Neuropharmacology. 1988 Oct;27(10):1045-53. doi: 10.1016/0028-3908(88)90066-4. PMID: 3070432.
