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Merck

M3262

Sigma-Aldrich

N-甲基- D -天冬氨酸

≥98% (TLC), suitable for cell culture

别名:

NMDA, (R)-2-(甲氨基)琥珀酸

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About This Item

经验公式(希尔记法):
C5H9NO4
CAS号:
分子量:
147.13
Beilstein:
1724431
MDL號碼:
分類程式碼代碼:
12352209
eCl@ss:
32160406
PubChem物質ID:
NACRES:
NA.32

product name

N-甲基- D -天冬氨酸, ≥98% (TLC), solid

化驗

≥98% (TLC)

形狀

solid

技術

cell culture | mammalian: suitable

顏色

white

mp

189-190 °C

應用

cell analysis

SMILES 字串

CN[C@H](CC(O)=O)C(O)=O

InChI

1S/C5H9NO4/c1-6-3(5(9)10)2-4(7)8/h3,6H,2H2,1H3,(H,7,8)(H,9,10)/t3-/m1/s1

InChI 密鑰

HOKKHZGPKSLGJE-GSVOUGTGSA-N

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一般說明

N-甲基-D-天冬氨酸(NMDA)是大鼠神经系统和内分泌腺中的内生分子。NMDA在腺垂体、下丘脑、脑和睾丸中以低水平(nmol/g)存在。NMDA通过S-腺苷甲硫氨酸依赖性酶(也称为NMDA合酶)对D-Asp衍生而来。

應用

N-甲基-D-天冬氨酸已用于诱导N-甲基-d-天冬氨酸(NMDA)的毒性,视网膜细胞培养物补充有NMDA。

生化/生理作用

N-甲基-D-天冬氨酸(NMDA)对于垂体中促黄体激素和PRL(催乳素),以及下丘脑中的GnRH(促性腺激素释放激素)的释放起着关键作用。它可作为NMDA型谷氨酸受体的特异性激动剂。
兴奋毒性氨基酸。NMDA型谷氨酸受体的原型激动剂,可调节离子通道;在长时程增强、缺血和癫痫中起重要作用。

儲存類別代碼

11 - Combustible Solids

水污染物質分類(WGK)

WGK 3

閃點(°F)

Not applicable

閃點(°C)

Not applicable

個人防護裝備

Eyeshields, Gloves, type N95 (US)


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Occurrence of D-aspartic acid and N-methyl-D-aspartic acid in rat neuroendocrine tissues and their role in the modulation of luteinizing hormone and growth hormone release.
D'Aniello A
Faseb Journal, 14(5), 699-714 (2000)
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Molecular neurobiology, 56(9), 6142-6155 (2019-02-09)
Mouse hippocampal glutamatergic nerve endings express presynaptic release-regulating NMDA autoreceptors (NMDARs). The presence of GluN1, GluN2A, GluN2B, and GluN3A subunits in hippocampal vesicular glutamate transporter type 1-positive synaptosomes was confirmed with confocal microscopy. GluN2C, GluN2D, and GluN3B immunopositivity was scarcely
N-methyl-D-aspartic acid (NMDA) in the nervous system of the amphioxus Branchiostoma lanceolatum.
D'Aniello S
BMC Neuroscience, 8:109 (2007)
Juan Ding et al.
Neural regeneration research, 14(12), 2112-2117 (2019-08-10)
N-methyl-D-aspartate receptor hypofunction is the basis of pathophysiology in schizophrenia. Blocking the N-methyl-D-aspartate receptor impairs learning and memory abilities and induces pathological changes in the brain. Previous studies have paid little attention to the role of the N-methyl-D-aspartate receptor subunit

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