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an alkaloid plant toxin extracted chiefly from nux vomica; formerly used as a stimulant

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ストリキニーネ(有毒の結晶で中枢神経の興奮剤)

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2013/12/27 12:13:32」(JST)

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Strychnine (/ˈstrɪkniːn/; also US /ˈstrɪknaɪn/ or /ˈstrɪknɪn/) is a highly toxic (LD₅₀ = 0.16 mg/kg in rats, 1–2 mg/kg orally in humans^[2]), colorless, bitter crystalline alkaloid used as a pesticide, particularly for killing small vertebrates such as birds and rodents. Strychnine, when inhaled, swallowed or absorbed through eyes or mouth, causes a poisoning which results in muscular convulsions and eventually death through asphyxia.^[3] The most common source is from the seeds of the Strychnos nux-vomica tree.

History[edit]

Strychnine was the first alkaloid to be identified in plants of the genus Strychnos, family Loganiaceae. Strychnos, named by Carl Linnaeus in 1753, is a genus of trees and climbing shrubs of the gentian order. The genus contains 196 various species and is distributed throughout the warm regions of Asia (58 species), America (64 species), and Africa (75 species). The seeds and bark of many plants in this genus contain the powerful poison strychnine.

The toxic and medicinal effects of Strychnos nux-vomica have been well known from the times of ancient China and India, although the chemical compound itself was not identified and characterized until the 19th century. The inhabitants of these countries had historical knowledge of the species Strychnos nux-vomica and Saint-Ignatius’ bean (Strychnos ignatii). Strychnos nux-vomica is a tree native to Indonesia which attains a height of 12 m. The tree has a crooked, short, thick trunk and the wood is close grained and very durable. The fruit has an orange color and is about the size of a large apple with a hard rind and contains five seeds, which are covered with a soft wool-like substance. The ripe seeds look like flattened disks, which are very hard. These seeds are the chief commercial source of strychnine and were first imported to and marketed in Europe as a poison to kill rodents and small predators. Strychnos ignatii is a woody climbing shrub of the Philippines. The fruit of the plant, known as Saint Ignatius' bean, contains as many as 25 seeds embedded in the pulp. The seeds contain more strychnine than other commercial alkaloids. The properties of S. nux-vomica and S. ignatii are substantially those of the alkaloid strychnine.

Strychnine was first discovered by French chemists Joseph Bienaimé Caventou and Pierre-Joseph Pelletier in 1818 in the Saint-Ignatius’ bean.^[4] In some Strychnos plants a 9,10-dimethoxy derivative of strychnine, the alkaloid brucine, is also present. Brucine is not as poisonous as strychnine. Historic records indicate that preparations containing strychnine (presumably) had been used to kill dogs, cats, and birds in Europe as far back as 1640^{[citation needed]}. The structure of strychnine was first determined in 1946 by Sir Robert Robinson and in 1954 this alkaloid was synthesized in a laboratory by Robert B. Woodward. This is one of the most famous syntheses in the history of organic chemistry. Both chemists won the Nobel prize (Robinson in 1947 and Woodward in 1965).^[5]

Biosynthesis[edit]

Strychnine is a terpene indole alkaloid belonging to the Strychnos family of Corynanthe alkaloids, and it is derived from tryptamine and secologanin.^[6]^[7] The enzyme, strictosidine synthase, catalyzes the condensation of tryptamine and secologanin, followed by a Pictet-Spengler reaction to form strictosidine.^[8] While the enzymes that catalyze the following steps have not been identified, the steps have been inferred by isolation of intermediates from Strychnos nux vomica.^[9] The next step is hydrolysis of the acetal, which opens the ring by elimination of glucose (O-Glu) and provides a reactive aldehyde. The nascent aldehyde is then attacked by a secondary amine to afford geissoschizine, a common intermediate of many related compounds in the Strychnos family.^[6]

A reverse Pictet-Spengler reaction cleaves the C2-C3 bond, while a subsequent Mannich reaction forms the C3-C7 bond, and a Michael addition forms the C2-C16 bond to provide dehydropreakuammicine. Hydrolysis of the methyl ester and decarboxylation leads to norfluorocurarine. Stereospecific reduction of the endocyclic double bond by NADPH and hydroxylation provides the Wieland-Gumlich aldehyde, which was first isolated by Heimberger and Scott in 1973, although previously synthesized by Wieland and Gumlich in 1932.^[9]^[10] To elongate the appendage by 2 carbons, acetyl-CoA is added to the aldehyde in an aldol reaction to afford prestrychnine. Stychnine is then formed by a facile addition of the amine with the carboxylic acid or its activated CoA thioester, followed by ring-closure via displacement of an activated alcohol.

Toxicokinetics[edit]

Strychnine may be introduced into the body orally, by inhalation, or by injection. It is rapidly absorbed from the gastrointestinal tract.

Distribution[edit]

Strychnine is transported by plasma and erythrocytes. Due to slight protein binding, strychnine leaves the bloodstream quickly and distributes to the tissues. Approximately 50% of the ingested dose can enter the tissues in 5 minutes. Also within a few minutes of ingestion, strychnine can be detected in the urine. Little difference was noted between oral and intramuscular administration of strychnine.^{[citation needed]} In persons killed by strychnine, the highest concentrations are found in the blood, liver, kidney and stomach wall. The usual fatal dose is 60–100 mg strychnine and is fatal after a period of 1–2 hours, though lethal doses vary depending on the individual.

Half-life[edit]

The biological half-life of strychnine is about 10 hours. This half-life suggests that normal hepatic function can efficiently degrade strychnine even when the quantity ingested is high enough to cause severe poisoning.

Metabolism[edit]

Strychnine is rapidly metabolized by the liver microsomal enzyme system requiring NADPH and O2. Strychnine competes with the inhibitory neurotransmitter glycine resulting in an excitatory state. However, the toxicokinetics after overdose have not been well described. In most severe cases of strychnine poisoning, the patient dies before reaching the hospital.

Elimination/excretion[edit]

A few minutes after ingestion, strychnine is excreted unchanged in the urine, and accounts for about 5 to 15% of a sublethal dose given over 6 hours. Approximately 10 to 20% of the dose will be excreted unchanged in the urine in the first 24 hours. The percentage excreted decreases with the increasing dose. Of the amount excreted by the kidneys, about 70% is excreted in the first 6 hours, and almost 90% in the first 24 hours. Excretion is almost complete in 48 to 72 hours.^[5]

Symptoms[edit]

Strychnine poisoning can be fatal to humans and animals and can occur by inhalation, swallowing or absorption through eyes or mouth, as explained above. It produces some of the most dramatic and painful symptoms of any known toxic reaction. For this reason, strychnine poisoning is often used in literature and film. It is also used as a rodenticide, but is not specific for unwanted pests and may kill other small animals. S. nux-vomica seeds are generally effective only when they are crushed or chewed before swallowing because the pericarp is quite hard and indigestible; poisoning symptoms may not appear if the seeds are ingested whole. The following symptoms are indicative of a lethal dose:

Severe nausea, including vomiting
Convulsions of all muscle groups, which become longer and more closely spaced with time
Spasms of the facial muscles, causing cyanosis of the face, dilated pupils, prominent eye balls, and frothing at the mouth
The body may be seen arch-shapes in following postures:
1. Opisthotonus: Hyperextension. The person may be resting on heels and occiput.
2. Emprosthotonos: The spasm of abdominal muscles may bend the body forward.
3. Pleurothotonus: The body may be flexed to one side.
Loss of consciousness and a clear mind
Immense reflex sensitivity (dramatic exaggeration of normal reflexes)
Death due to asphyxiation, caused by muscle spasms^[3]

Mechanism[edit]

Strychnine is a neurotoxin which acts as an antagonist of glycine and acetylcholine receptors. It primarily affects the motor nerves in the spinal cord which control muscle contraction. An impulse is triggered at one end of a nerve by the binding of neurotransmitters to the receptors. In the presence of neuroinhibitors, a greater quantity of neurotransmitters must bind to receptors before there will be an action potential generated. An example of a neurotransmitter is glycine, which acts primarily as an agonist of the glycine receptor. This is a ligand-gated chloride channel in neurons located in the spinal cord and in the brain. Strychnine is an antagonist of glycine, which means it binds to the same receptor. When strychnine binds to this receptor, glycine is unable to bind to it at the same time. Therefore, the inhibiting effect of glycine is reduced, so nerve impulses are triggered with lower levels of neurotransmitters. When there is no inhibitory effect the motor neurons do not stop their activity and the victim will have constant muscle contractions.^[11] Structure of strychnine in complex with ACh binding protein (AChBP).^[12]

Strychnine is also an antagonist for acetylcholine receptors,^[13] which is known to be homologous to the glycine receptor.

In low dosages, strychnine can act as a stimulant and has been used by athletes to enhance their performance. Strychnine made headlines back in 1904 during the St. Louis Olympics. At that time there were no rules yet about the use of performance enhancing drugs. The American Fred Lorz won the marathon competition but was disqualified just after crossing the finish line because officials learned he had taken a car ride for part of the race. The next man to finish was the British-born US athlete Thomas Hicks. He won the gold medal but not without a little help. About 10 miles from the finish line Hicks begged his trainers to let him stop running and give-up the race. His trainers refused and gave him a dose of strychnine as a stimulant to keep him going. They also gave him raw egg-white and brandy. As a result Hicks had to be carried across the finish line and it took four doctors to revive him so that he could leave the stadium. More recently at the 1992 Barcelona Olympics, strychnine was used to optimize the athletic performance of Wu Dan, a female volleyball player from China. Dan was the first person to test positive for drugs at the Olympics, testing positive for strychnine despite claiming that she had not ingested any. The strychnine was contained in capsules that Dan was taking without the knowledge of the team doctor. She took the capsule as a tonic because she was feeling a bit tired. The Olympic committee banned her from any more competition but stated that Dan didn’t intentionally cheat.^[14]

Animal toxicity[edit]

Strychnine poisoning in animals occurs usually from ingestion of baits designed for use against gophers, moles and coyotes. Since 1990 in the United States most baits containing strychnine have been replaced with zinc phosphide baits. In the Netherlands rodenticides with strychnine are forbidden. Strychnine toxicity in rats is dependent on sex. It is more toxic to females than to males when administered via subcutaneous injection or intraperitoneal injection. Differences are due to higher rates of metabolism by male rat liver microsomes. Dogs and cats are more susceptible among domestic animals, pigs are believed to be as susceptible as dogs, and horses are able to tolerate relatively large amounts of strychnine. Birds affected by strychnine poisoning exhibit wing droop, salivation, tremors, muscle tenseness and convulsions. Death occurs as a result of respiratory arrest. The clinical signs of strychnine poisoning relate to its effects on the central nervous system. The first clinical signs of poisoning include nervousness, restlessness, twitching of the muscles, and stiffness of the neck. As the poisoning progresses, the muscular twitching becomes more pronounced and convulsions suddenly appear in all the skeletal muscles. The limbs are extended and the neck is curved to opisthotonus. The pupils are widely dilated. As death approaches, the convulsions follow one another with increased rapidity, severity, and duration. Death results from asphyxia due to prolonged paralysis of the respiratory muscles. Following the ingestion of strychnine, symptoms of poisoning usually appear within 15 to 60 min. The LD₅₀-values for strychnine in animals are listed below in table 1.

The LD₅₀ values for strychnine in animals
Organism	Route	LD₅₀ (mg/kg)
Bird-wild^[15]	Oral	16
Cat^[16]	Intravenous	0.33
Cat^[17]	Oral	0.5
Dog^[18]	Intravenous	0.8
Dog^[16]	Subcutaneous	0.35
Dog^[17]	Oral	0.5
Duck^[15]	Oral	3.0
Mouse^[19]	Intraperitoneal	0.98
Mouse^[20]	Intravenous	0.41
Mouse^[21]	Oral	2.0
Mouse^[22]	Parenteral	1.06
Mouse^[23]	Subcutaneous	0.47
Pigeon^[15]	Oral	21.0
Quail^[15]	Oral	23.0
Rabbit^[18]	Intravenous	0.4
Rabbit^[16]	Oral	0.6
Rat^[24]	Oral	16.0
Rat^[25]	Oral	2.35

Human toxicity[edit]

Strychnine is very toxic to humans and many other animals; the symptoms of poisoning are generally the same as in other animals, because the mechanism of action is apparently similar across different species. Due to ethical reasons, the toxicity of strychnine in humans has not been widely studied. Most of the information known today comes from real-life cases of strychnine poisoning, both unintentional and deliberate. The LD₅₀-values estimated from different cases of strychnine poisoning are listed below in table 2.

The LD₅₀ values for strychnine in humans
	Route	LD₅₀ (mg)
Human^[26]^[27]	Oral	100-120
Human^[28]	Oral	30-60
Human (child)^[29]^[30]^[31]	Oral	15
Human (adult)^[32]	Oral	50-100
Human (adult)^[31]	Oral	30-100
Human (adult)^[30]	Oral	30
Human^[33]	Intravenously	5-10 (approximate)

For occupational exposures to strychnine, the Occupational Safety and Health Administration and National Institute for Occupational Safety and Health have set exposure limits at 0.15 mg/m³ over an 8-hour work day.^[34]

Treatment[edit]

There is no specific antidote for strychnine but recovery from strychnine exposure is possible with early hospital treatment. Treatment consists of removing the drug from the body (decontamination) and getting supportive medical care in a hospital setting. Supportive care includes intravenous fluids, medications against convulsions and spasms, and cooling measures for high temperature. The patient should be kept in a quiet and darkened room, because excessive manipulation and loud noises may cause convulsions. Because these convulsions are extremely painful, an appropriate painkiller should be given. Treatment of strychnine poisoning involves an oral administration of activated charcoal which adsorbs any strychnine within the digestive tract. Unabsorbed strychnine can be removed from the stomach by gastric lavage with tannic acid or potassium permanganate solutions to oxidize strychnine. Seizures are controlled by anticonvulsants, such as phenobarbital or diazepam, along with muscle relaxants such as dantrolene to combat muscle rigidity. Chloroform or heavy doses of chloral, bromide, urethane or amyl nitrate can also be used to restrain the convulsions. Because diazepam, as the anticonvulsant of choice, is not effective in all cases, a combination with midazolam, fentanyl, or pancuronium is recommended for controlling the convulsions. The fatal outcome of strychnine poisoning demands an aggressive management with early intubation, control of muscle tremors, and prevention of rhabdomyolysis and renal failure. If the patient survives the first 24 hours after poisoning then recovery is probable.

Bitterness[edit]

Strychnine is a potently bitter substance. In humans, it activates bitter taste receptors TAS2R10 and TAS2R46.^[35]^[36]

References[edit]

^ Everett, A. J.; Openshaw, H. T.; Smith, G. F. (1957). "221. The constitution of aspidospermine. Part III. Reactivity at the nitrogen atoms, and biogenetic considerations". Journal of the Chemical Society (Resumed): 1120. doi:10.1039/JR9570001120. edit
^ INCHEM: Chemical Safety Information from Intergovernmental Organizations:Strychnine. http://www.inchem.org/documents/pims/chemical/pim507.htm
^ ^a ^b Sharma, R.K., Consice textbook of forensic medicine & toxicology, Elsevier, 2008
^ Pelletier and Caventou (1818) "Note sur un nouvel alkalai" (Note on a new alkali), Annales de Chimie et de Physique, vol. 8, pages 323-324. See also: Pelletier and Caventou (1819) "Mémoire sur un nouvel alcali vegetal (la strychnine) trouvé dans la feve de Saint-Ignace, la noix vomique, etc." (Memoir on a new vegetable alkali (strychnine) found in the St. Ignatius bean, the nux vomica, etc), Annales de Chimie et de Physique, vol. 10, pages 142 - 176.
^ ^a ^b Gupta, R.C., Handbook of Toxicology of Chemical Warfare Agents, Elsevier Inc, 2009, Chapter 14
^ ^a ^b Bonjoch, Josep; Solé, Daniel (1 September 2000). "Synthesis of Strychnine". Chemical Reviews 100 (9): 3455–3482. doi:10.1021/cr9902547. Cite uses deprecated parameters (help)
^ Dewick, Paul M. (2009). Medicinal natural products : a biosynthetic approach (3rd ed. ed.). Chichester: A John Wiley & Sons. pp. 377–378. ISBN 978-0-470-74167-2.
^ Treimer, Johannes F.; Zenk, Meinhart H. (1 November 1979). "Purification and Properties of Strictosidine Synthase, the Key Enzyme in Indole Alkaloid Formation". European Journal of Biochemistry 101 (1): 225–233. doi:10.1111/j.1432-1033.1979.tb04235.x. PMID 510306. Cite uses deprecated parameters (help)
^ ^a ^b Heimberger, Stanley I.; Scott, A. Ian (1 January 1973). "Biosynthesis of strychnine". Journal of the Chemical Socie ty, Chemical Communications (6): 217. doi:10.1039/C39730000217. Cite uses deprecated parameters (help)
^ Wieland, Heinrich; Gumlich, Walter (1 January 1932). "Über einige neue Reaktionen der Strychnos - Alkaloide. XI". Justus Liebig's Annalen der Chemie 494 (1): 191–200. doi:10.1002/jlac.19324940116. Cite uses deprecated parameters (help)
^ Waring, R.H., Steventon, G.B, Mitchell, S.C, Molecules of death, Imperial College Press, 2007
^ Brams et al. (2011). "A structural and mutagenic blueprint for molecular recognition of strychnine and d-tubocurarine by different cys-loop receptors". PLoS Biol 9 (3). doi:10.1371/journal.pbio.1001034.
^ Daly JW (June 2005). "Nicotinic agonists, antagonists, and modulators from natural sources". Cell. Mol. Neurobiol. 25 (3-4): 513–52. doi:10.1007/s10571-005-3968-4. PMID 16075378. Cite uses deprecated parameters (help)
^ Rios, D., Strychnine, 2007
^ ^a ^b ^c ^d Tucker, RK; Haegele, MA (1971). "Comparative acute oral toxicity of pesticides to six species of birds". Toxicology and applied pharmacology 20 (1): 57–65. doi:10.1016/0041-008X(71)90088-3. PMID 5110827.
^ ^a ^b ^c RTECS (1935)
^ ^a ^b Moraillon, R.; Pinoult, L. (1978). "Diagnostic et traitement d'intoxications courantes des carnivores". Rec Med Vet (in French) 174 (1–2): 36–43.
^ ^a ^b Longo, V.G.; Silvestrini, B.; Bovet, D. (1959). "An investigation of convulsant properties of the 5,7-diphenyl-1,3-diazadamantan- 6-ol (IS 1757)". J. Pharmacol. Exp. Ther. 126 (1): 41–9. PMID 13642285.
^ Setnikar, I; Murmann, W; Magistretti, MJ; Da Re, P (1960). "Amino-methylchromones, brain stem stimulants and pentobarbital antagonists". The Journal of Pharmacology and Experimental Therapeutics 128: 176–81. PMID 14445192.
^ Haas, H (1960). "On 3-piperidino-1-phenyl-1-bicycloheptenyl-1-propanol (Akineton). 2". Archives internationales de pharmacodynamie et de therapie 128: 204–38. PMID 13710192.
^ Prasad, CR; Patnaik, GK; Gupta, RC; Anand, N; Dhawan, BN (1981). "Central nervous system stimulant activity of n-(delta 3-chromene-3-carbonyl)-4 iminopyridine (compound 69/224)". Indian journal of experimental biology 19 (11): 1075–6. PMID 7338366.
^ Zapata-Ortiz, V; CASTRO DE LA MATA R; Barantes-Campos, R (1961). "The anticonvulsive action of cocaine". Arzneimittel-Forschung 11: 657–62. PMID 13787891.
^ Sandberg, F; Kristianson, K (1970). "A comparative study of the convulsant effects of strychnos alkaloids". Acta pharmaceutica Suecica 7 (4): 329–36. PMID 5480076.
^ Spector, W.S. (1956). Handbook of Toxicology, Vol. 1, p. 286. W.B. Saunders Company, Philadelphia.
^ Ward, Justus C.; Crabtree, D. Glen (2006). "Strychnine X. Comparative accuracies of stomach tube and intraperitoneal injection methods of bioassay". Journal of the American Pharmaceutical Association 31 (4): 113–115. doi:10.1002/jps.3030310406.
^ Zenz, C., Dickerson, O.B., Horvath, E.P. (1994). Occupational Medicine, 3rd edition, p. 640. St Louis.
^ Palatnick, W; Meatherall, R; Sitar, D; Tenenbein, M (1997). "Toxicokinetics of acute strychnine poisoning". Journal of toxicology. Clinical toxicology 35 (6): 617–20. PMID 9365429.
^ Lewis, R.J. (1996). Sax’s Dangerous Properties of Industrial Materials. 9th edition, Vols 1–3, p. 3025. Van Nostrand Reinhold, New York.
^ Goodman, L.S, Gilman, A.G, Gilman A. The pharmalogical basis of therapeutics, 1985, New York Macmillan Publishing & Co., Inc.
^ ^a ^b Bennett, S.M. http://www.the-piedpiper.co.uk/th15\%28f\%29.htm
^ ^a ^b Gossel, T.A., Bricker J.D. (1994). Principles of Clinical Toxicology,3rd edition, p. 351. Raven Press, New York.
^ Migliaccio, E; Celentano, R; Viglietti, A; Viglietti, G (1990). "Strychnine poisoning. A clinical case". Minerva anestesiologica 56 (1–2): 41–2. PMID 2215981.
^ Ellenhorn, M.J., Schonwald, S., Ordog, G. (1997). J. Wasserberger. Ellenhorn’s Medical Toxicology: Diagnosis and Treatment of Human Poisoning, 2nd edition, p. 1660. Williams and Wilkins, Baltimore.
^ CDC - NIOSH Pocket Guide to Chemical Hazards
^ Meyerhof, W.; Batram, C.; Kuhn, C.; Brockhoff, A.; Chudoba, E.; Bufe, B.; Appendino, G.; Behrens, M. (2009). "The Molecular Receptive Ranges of Human TAS2R Bitter Taste Receptors". Chemical Senses 35 (2): 157–170. doi:10.1093/chemse/bjp092. PMID 20022913. edit
^ "BitterDB - Strychnine". Hebrew University of Jerusalem. Retrieved 11 June 2013.

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English Journal

Novel limonene and citral based 2,5-disubstituted-1,3,4-oxadiazoles: A natural product coupled approach to semicarbazones for antiepileptic activity.

Rajak H, Singh Thakur B, Singh A, Raghuvanshi K, Sah AK, Veerasamy R, Sharma PC, Singh Pawar R, Kharya MD.SourceMedicinal Chemistry Research Laboratory, SLT Institute of Pharmaceutical Sciences, Guru Ghasidas University, Bilaspur 495 009, CG, India. Electronic address: harishdops@yahoo.co.in.
Bioorganic & medicinal chemistry letters.Bioorg Med Chem Lett.2013 Feb 1;23(3):864-8. doi: 10.1016/j.bmcl.2012.11.051. Epub 2012 Nov 27.
Two novel series of N(4)-(5-(2/3/4-substituted-phenyl)-1,3,4-oxadiazol-2-yl)-N(1)-(2-methyl-5-(prop-1-en-2-yl)cyclohex-2-enylidene)semicarbazide and N(4)-(5-(2/3/4-substituted-phenyl)-1,3,4-oxadiazol-2-yl)-N(1)-(3,7-dimethylocta-3,6-dienylidene)-semicarbazide were synthesized to meet structural prer
PMID 23265873

Spontaneous glycine-induced calcium transients in spinal cord progenitors promote neurogenesis.

Brustein E, Côté S, Ghislain J, Drapeau P.SourceDepartment of Pathology and Cell Biology and "Groupe de recherche sur le système nerveux central," University of Montreal, Montreal, Quebec H3C 3J7, Canada.
Developmental neurobiology.Dev Neurobiol.2013 Feb;73(2):168-75. doi: 10.1002/dneu.22050. Epub 2012 Oct 17.
Glycine and GABA are depolarizing during early development, but the purpose of this paradoxical chloride-mediated depolarization remains unclear, especially at early stages. It was previously reported that suppressing glycine signaling from the beginning of development in zebrafish embryos caused an
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Alpha-asarone from Acorus gramineus alleviates epilepsy by modulating A-Type GABA receptors.

Huang C, Li WG, Zhang XB, Wang L, Xu TL, Wu D, Li Y.SourceInstitute of Chinese Materia Medica, Shanghai University of Traditional Chinese Medicine, 1200 Cailun Road, Shanghai 201203, China; Neuroscience Division, Department of Biochemistry and Molecular Cell Biology, Institute of Medical Sciences, Shanghai Jiao Tong University School of Medicine, 280 South Chongqing Road, Shanghai 200025, China.
Neuropharmacology.Neuropharmacology.2013 Feb;65:1-11. doi: 10.1016/j.neuropharm.2012.09.001. Epub 2012 Sep 10.
Alpha (α)-asarone is a major effective compound isolated from the Chinese medicinal herb Acorus gramineus, which is widely used in clinical practice as an antiepileptic drug; however, its mechanism of action remains unclear. In this study, we have characterized the action of α-asarone on the excit
PMID 22975146

Japanese Journal

Orexin neurons receive glycinergic innervations

Hondo Mari,Furutani Naoki,Yamasaki Miwako,Watanabe Masahiko,Sakurai Takeshi
PLoS ONE 6(9), e25076, 2011-09-16
… These responses were inhibited by a specific glycine receptor antagonist, strychnine. …
NAID 120003497597

HPLC Determination of Strychnine and Brucine in Rat Tissues and the Distribution Study of Processed Semen Strychni

CHEN Jun,HOU Ting,FANG Yun,CHEN Zhi-peng,LIU Xiao,CAI Hao,LU Tu-lin,YAN Guo-jun,CAI Bao-chang
YAKUGAKU ZASSHI 131(5), 721-729, 2011
… A simple and low-cost HPLC method with UV absorbance detection was developed and validated to simultaneously determine strychnine and brucine, the most abundant alkaloids in the processed Semen Strychni, in rat tissues (kidney, liver, spleen, lung, heart, stomach, small intestine, brain and plasma). … Then the method was used to measure the tissue distribution of strychnine and brucine after intravenous administration of 1 mg/kg crude alkaloids fraction (CAF) extracted from the processed Semen Strychni. …
NAID 130000678854

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「ストリキニーネ」

Strychnine
	Other names Strychnidin-10-one
Identifiers
CAS number	57-24-9 (base) , 60-41-3 (sulfate)
PubChem	441071
ChemSpider	389877
UNII	H9Y79VD43J
KEGG	C06522
ChEBI	CHEBI:28973
ChEMBL	CHEMBL227934 , CHEMBL612118, CHEMBL486399
Jmol-3D images	Image 1
	SMILES O=C7N2c1ccccc1[C@@]64[C@@H]2[C@@H]3[C@@H](OC/C=C5\[C@@H]3C[C@@H]6N(CC4)C5)C7 ;
	InChI InChI=1S/C21H22N2O2/c24-18-10-16-19-13-9-17-21(6-7-22(17)11-12(13)5-8-25-16)14-3-1-2-4-15(14)23(18)20(19)21/h1-5,13,16-17,19-20H,6-11H2/t13-,16-,17-,19-,20-,21+/m0/s1 ; Key: QMGVPVSNSZLJIA-FVWCLLPLSA-N InChI=1/C21H22N2O2/c24-18-10-16-19-13-9-17-21(6-7-22(17)11-12(13)5-8-25-16)14-3-1-2-4-15(14)23(18)20(19)21/h1-5,13,16-17,19-20H,6-11H2/t13-,16-,17-,19-,20-,21+/m0/s1; Key: QMGVPVSNSZLJIA-FVWCLLPLBR ;
Properties
Molecular formula	C21H22N2O2
Molar mass	334.41 g mol−1
Appearance	white or translucent cristal or crystilline powder; Bitter tasting
Odor	Odorless
Density	1.36 g cm−3
Melting point	543 K (270 °C)
Boiling point	557−559 K (284−286 °C)
Acidity (pKa)	8.25
	(verify) (what is: /?); Except where noted otherwise, data are given for materials in their standard state (at 25 °C (77 °F), 100 kPa)
	Infobox references

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英: strychnine
ラ: strychninum
同: ストリキニン
化: 硝酸ストリキニーネ strychnini nitras
商: ホミカエキス
関

痙攣薬
アルカロイド

薬理作用

SPC.210

グリシン受容体の拮抗阻害薬
脊髄の抑制物質であるグリシンに拮抗することで、Renshaw細胞のネガティブフィードバックを解除する→興奮↑

中毒症状