Methylazoxymethanol acetate
Chemical compound
From Wikipedia, the free encyclopedia
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] It is an acetate of methylazoxymethanol.
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| Names | |||
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| IUPAC name | |||
| Preferred IUPAC name
[(Z)-methyl-ONN-azoxy]methyl acetate | |||
| Other names
MAM | |||
| Identifiers | |||
3D model (JSmol) |
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| ChEBI | |||
| ChemSpider | |||
| ECHA InfoCard | 100.008.879 | ||
| EC Number |
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| KEGG | |||
| MeSH | D008746 | ||
PubChem CID |
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| UNII | |||
CompTox Dashboard (EPA) |
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| Properties | |||
| C4H8N2O3 | |||
| Molar mass | 132.11792 | ||
| Hazards | |||
| GHS labelling: | |||
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| Danger | |||
| H350, H360D | |||
| P201, P202, P281, P308+P313, P405, P501 | |||
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
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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]