メチルアゾキシメタノール・酸

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a salt or ester of acetic acid (同)ethanoate

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酢酸(さくさん)塩;アセテート(酢酸人造絹糸)

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2017/06/19 02:44:59」(JST)

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Methylazoxymethanol acetate, MAM, is a neurotoxin which reduces DNA synthesis^[1] used in making animal models of neurological diseases including schizophrenia^[2] and epilepsy.^[3] MAM is found in cycad seeds, and causes zamia staggers. It selectively targets neuroblasts in the central nervous system. In rats, administration of MAM affects structures in the brain which are developing most quickly.^[2]

MAM animal models

Schizophrenia

In rat models, the specific effect of MAM on neural development depends on the gestational age of the subject. At the seventeenth gestational day (GD17), administration of MAM produces behavioral and histopathological patterns found in schizophrenia.^[2] The molecular mechanism behind this model is not fully known.^[4] Methylazoxymethanol acetate administered at GD17 reduces the thickness of the hippocampus and the thalamus. The locomotor effects of amphetamines and the spontaneous firing rate of dopaminergic neurons in the ventral tegmental area are increased. In alternating maze tests, GD17 MAM rats quickly learned the first rule, but took longer to accommodate to alterations to the rule; this is thought to indicate deficits in working spatial memory, which is also impaired in schizophrenia.^[2]

Epilepsy

Exposure to MAM before birth increases susceptibility to epileptic seizures caused by flurothyl.^[3] Prenatal MAM exposure in rats results in a model of brain malformation. In some MAM animals, video-EEG monitoring has documented the presence of spontaneous electrographic seizure activity ^[5] In some epilepsy rat models, MAM is administered at the fifteenth gestational day. Previous studies have found impaired cognitive function in GD15 MAM rats, and a reduced seizure threshold.^[6] At the cellular level, dysplastic hippocampal neurons in the MAM model were shown to have reduced potassium current function and expression for the Kv4.2 channel subunit ^[7] These findings may contribute to the spontaneous seizures and reduced seizure thresholds seen in this model.

References

^ "Methylazoxymethanol Acetate – Compound Summary". PubChem. National Center for Biotechnology Information. Retrieved 9 June 2012.
^ ^a ^b ^c ^d Jones, CA; Watson, DJG; Fone, KCF (1 October 2011). "Animal models of schizophrenia". British Journal of Pharmacology. 164 (4): 1162–1194. PMC 3229756 . PMID 21449915. doi:10.1111/j.1476-5381.2011.01386.x.
^ ^a ^b Baraban, Scott C.; Schwartzkroin, Philip A. (31 March 1996). "Flurothyl seizure susceptibility in rats following prenatal methylazoxymethanol treatment". Epilepsy Research. 23 (3): 189–194. doi:10.1016/0920-1211(95)00094-1.
^ Hradetzky, Eva; et al. (28 September 2011). "The Methylazoxymethanol Acetate (MAM-E17) Rat Model: Molecular and Functional Effects in the Hippocampus". Neuropsychopharmacology. 37 (2): 364–377. PMC 3242314 . PMID 21956444. doi:10.1038/npp.2011.219.
^ Harrington, Emily; et al. (January 2007). "Altered glutamate receptor-transporter and spontaneous seizures in rats exposed to methylazoxymethanol in utero". Epilepsia. 48 (1): 158–168. PMID 17241223. doi:10.1111/j.1528-1167.2006.00838.x.
^ Moshé, editors, Asla Pitkänen, Philip A. Schwartzkroin, Solomon L. (2006). Models of seizures and epilepsy. Amsterdam: Elsevier Academic. pp. 305–312. ISBN 0120885549.
^ Castro, Peter; et al. (1 September 2001). "AHippocampal heterotopia lack functional Kv4.2 potassium channels in the methylazoxymethanol model of cortical malformations and epilepsy.". Journal of Neuroscience. 21 (17): 6626–6634. doi:10.1111/j.1528-1167.2011.03264.x.

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English Journal

Social Interaction Rescues Memory Deficit in an Animal Model of Alzheimer's Disease by Increasing BDNF-Dependent Hippocampal Neurogenesis.

Hsiao YH1, Hung HC2, Chen SH3, Gean PW4.
The Journal of neuroscience : the official journal of the Society for Neuroscience.J Neurosci.2014 Dec 3;34(49):16207-19. doi: 10.1523/JNEUROSCI.0747-14.2014.
It has been recognized that the risk of cognitive decline during aging can be reduced if one maintains strong social connections, yet the neural events underlying this beneficial effect have not been rigorously studied. Here, we show that amyloid precursor protein (APP) and presenilin 1 (PS1) double
PMID 25471562

An augmented dopamine system function is present prior to puberty in the methylazoxymethanol acetate rodent model of schizophrenia.

Chen L1, Perez SM, Lodge DJ.
Developmental neurobiology.Dev Neurobiol.2014 Sep;74(9):907-17. doi: 10.1002/dneu.22172. Epub 2014 Mar 3.
Schizophrenia is a disease typically associated with an adolescent onset. Although there have been a considerable number of imaging studies investigating the transition to psychosis in prodromal patients, there are relatively few preclinical studies examining potential mechanisms that may contribute
PMID 24554310

Vagal nerve stimulation reverses aberrant dopamine system function in the methylazoxymethanol acetate rodent model of schizophrenia.

Perez SM1, Carreno FR1, Frazer A2, Lodge DJ3.
The Journal of neuroscience : the official journal of the Society for Neuroscience.J Neurosci.2014 Jul 9;34(28):9261-7. doi: 10.1523/JNEUROSCI.0588-14.2014.
Vagal nerve stimulation (VNS) is an alternative therapy for epilepsy and treatment refractory depression. Here we examine VNS as a potential therapy for the treatment of schizophrenia in the methylozoxymethanol acetate (MAM) rodent model of the disease. We have previously demonstrated that hyperacti
PMID 25009259

Japanese Journal

Regeneration of 5-HT fibers in hippocampal heterotopia of methylazoxymethanol-induced micrencephalic rats after neonatal 5,7-DHT injection

NAKAMURA Arata,KADOWAKI Taro,SAKAKIBARA Shin-ichi,YOSHIMOTO Kanji,HIRATA Koichi,UEDA Shuichi
Anatomical science international 85(1), 38-45, 2010-03-01
NAID 10027191167

Initiation and spread of epileptiform discharges in the methylazoxymethanol acetate rat model of cortical dysplasia : functional and structural connectivity between CA1 heterotopia and hippocampus/neocortex

TSCHULUUN N
Neuroscience 133, 327-342, 2005
NAID 30008329094

「メチルアゾキシメタノール酢酸」

Methylazoxymethanol acetate
Names
	IUPAC name (Z)-acetyloxymethylimino-methyl-oxidoazanium
	Other names MAM
Identifiers
3D model (JSmol)	Interactive image;
ChemSpider	19953632;
ECHA InfoCard	100.008.879
EC Number	209-765-7
KEGG	C19258;
MeSH	D008746
PubChem CID	5363199;
	InChI InChI=1S/C4H8N2O3/c1-4(7)9-3-5-6(2)8/h3H2,1-2H3/b6-5- Key: BELPJCDYWUCHKF-WAYWQWQTSA-N ; InChI=1/C4H8N2O3/c1-4(7)9-3-5-6(2)8/h3H2,1-2H3/b6-5- Key: BELPJCDYWUCHKF-WAYWQWQTBQ ;
	SMILES CC(=O)OC/N=[N+](/C)\[O-] ;
Properties
Chemical formula	C4H8N2O3
Molar mass	132.11792
	Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
	Infobox references

　　[★]

英: methylazoxymethanol acetate

[PubChem-1] "Methylazoxymethanol Acetate – Compound Summary". PubChem. National Center for Biotechnology Information. Retrieved 9 June 2012.

[jones-2] Jones, CA; Watson, DJG; Fone, KCF (1 October 2011). "Animal models of schizophrenia". British Journal of Pharmacology. 164 (4): 1162–1194. PMC 3229756 . PMID 21449915. doi:10.1111/j.1476-5381.2011.01386.x.

[baraban-3] Baraban, Scott C.; Schwartzkroin, Philip A. (31 March 1996). "Flurothyl seizure susceptibility in rats following prenatal methylazoxymethanol treatment". Epilepsy Research. 23 (3): 189–194. doi:10.1016/0920-1211(95)00094-1.

[4] Hradetzky, Eva; et al. (28 September 2011). "The Methylazoxymethanol Acetate (MAM-E17) Rat Model: Molecular and Functional Effects in the Hippocampus". Neuropsychopharmacology. 37 (2): 364–377. PMC 3242314 . PMID 21956444. doi:10.1038/npp.2011.219.

[5] Harrington, Emily; et al. (January 2007). "Altered glutamate receptor-transporter and spontaneous seizures in rats exposed to methylazoxymethanol in utero". Epilepsia. 48 (1): 158–168. PMID 17241223. doi:10.1111/j.1528-1167.2006.00838.x.

[6] Moshé, editors, Asla Pitkänen, Philip A. Schwartzkroin, Solomon L. (2006). Models of seizures and epilepsy. Amsterdam: Elsevier Academic. pp. 305–312. ISBN 0120885549.

[7] Castro, Peter; et al. (1 September 2001). "AHippocampal heterotopia lack functional Kv4.2 potassium channels in the methylazoxymethanol model of cortical malformations and epilepsy.". Journal of Neuroscience. 21 (17): 6626–6634. doi:10.1111/j.1528-1167.2011.03264.x.

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methylazoxymethanol acetate