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Merck
CN

324378

Domoic Acid, Mytilus edulis - CAS 14277-97-5 - Calbiochem

别名:

25-[2α, 3β, 4β (1Z, 3E, 5R)]-2-Carboxy-4-(5-carboxy-1-methyl-1,3-hexadienyl)-3-pyrrolidineacetic Acid

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assay

≥95% (HPLC)

form

crystalline solid

color

white to off-white

solubility

methanol: 0.6 mg/mL, H2O: 8 mg/mL

Quality Level

General description

A heat-stable neurotoxin. Glutamate kainate receptor agonist that shows higher affinity for the kainate receptor than any other known kainic acid analog. Causes excessive excitation of neurons resulting in the depletion of energy stores, cellular edema, and death. Inhibits adenylate cyclase activity in neuronal membranes. Evokes Ca2+-dependent and Ca2+-independent release of GABA.
Glutamate kainate excitatory amino acid agonist with the highest affinity for the kainate receptor of all known kainic acid analogs. It has been used to purify the kainate receptor by affinity chromatography. Its binding to the receptor causes continuous stimulation of nerve cells leading to depletion of energy, cellular edema, and death. Its neurological effect resembles anterograde memory loss associated with Alzheimer′s disease. Inhibits adenylate cyclase activity in brain membranes. Evokes Ca2+-dependent and Ca2+-independent release of GABA.

Biochem/physiol Actions

Glutamate kainate receptor

Preparation Note

Following reconstitution, store in the refrigerator (4°C). Do not freeze solutions. Stock solutions are stable for up to 24 h at 4°C.

存储类别

10-13 - German Storage Class 10 to 13

法规信息

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P N Usherwood et al.
Comparative biochemistry and physiology. C, Comparative pharmacology and toxicology, 103(1), 19-22 (1992-09-01)
1. A review is presented of recent advances in glutamate receptor research with particular emphasis on studies which show that some glutamate receptors in the central nervous systems (CNS) of Xenopus and rat contain a mixture of N-methyl-D-aspartate-sensitive and kainate-sensitive
R A Tasker et al.
Canadian journal of physiology and pharmacology, 69(3), 378-382 (1991-03-01)
Domoic acid, a structural analogue of kainic acid, has been identified as the toxin that poisoned people who consumed contaminated blue mussels harvested from eastern Prince Edward Island in December of 1987. To investigate the pharmacology of domoic acid in
G R Stewart et al.
Experimental neurology, 110(1), 127-138 (1990-10-01)
Domoic acid (Dom), a rigid analog of the excitotoxic amino acids, glutamate and kainic acid, is believed to be the mussel neurotoxin responsible for a recent food poisoning incident in Canada that killed some people and left others with memory
M Alfonso et al.
Neurochemistry international, 24(3), 267-274 (1994-03-01)
The effect of the neurotoxin domoic acid (DOM), a structural analogue of kainic acid, on the release of [3H]gamma-aminobutyric acid (GABA) and on the [Ca2+]i was studied in cultured chick retina cells. DOM stimulated dose-dependently the release of [3H]GABA with
M S Nijjar et al.
Molecular and cellular biochemistry, 136(2), 105-111 (1994-07-27)
Adenylate cyclase activity measured by the formation of cyclic AMP in rat brain membranes was inhibited by a shellfish toxin, domoic acid (DOM). The inhibition of enzyme was dependent on DOM concentration, but about 50% of enzyme activity was resistant

相关内容

Glutamate is an excitatory neurotransmitter found in the synaptic vesicles of glutamatergic synapses. The post-synaptic neurons in these synapses contain ionotropic and metabotropic glutamate receptors. Glutamate binds to AMPA (α-amino-3-hydroxy-5- methylisoxazole-4-propionic acid) subtype glutamate receptors, leading to sodium influx into the post-synaptic cell and resulting in neuronal excitability and synaptic transmission. The NMDA (N-methyl-d-aspartate) subtype glutamate receptors, on the other hand, regulate synaptic plasticity, and can influence learning and memory. The metabotropic g-protein coupled mGluRs modulate downstream calcium signaling pathways and indirectly influence the synapse’s excitability. The synaptic architecture includes intracellular scaffolding proteins (PSD-95, GRIP), intercellular cell adhesion molecules (NCAMs, N-Cadherins), and a variety of signaling proteins (CaMKII/PKA, PP1/PP2B). Processes critical for synaptic transmission and plasticity are influenced by these molecules and their interactions. When the function of these molecules is disrupted, it leads to synaptic dysfunction and degeneration, and can contribute to dementia as seen in Alzheimer’s disease.

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