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Historic kainate/quisqualate selective antagonist; may be able to distinguish between AMPA and kainate receptors. Anticonvulsant.
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The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.
References are publications that support the biological activity of the product.
Croucher et al (1984) γ-D-Glutamylaminomethylsulphonic acid (GAMS), a kainate and quisqualate antagonist, prevents sound-induced seizures in DBA/2 mice. Brain Res. 322 111 PMID: 6097331
Wilding and Huettner (1996) Antagonist pharmacology of kainate- and α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid-preferring receptors. Mol.Pharmacol. 49 540 PMID: 8643094
Zhou et al (1993) γ-D-Glutamylaminomethyl sulfonic acid (GAMS) distinguishes kainic acid- from AMPA-induced response in Xenopus oocytes expressing chick brain glutamate receptors. Neuropharmacology 32 767 PMID: 7692340
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Keywords: GAMS, GAMS supplier, Non-selective, Ionotropic, Glutamate, 0150, Tocris Bioscience
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Literature in this Area
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Epilepsy is a brain disease that affects 60 million people globally. More than 20 anti-seizure drugs are currently available, but these do not address the underlying causes of the condition. This poster summarizes current knowledge about the development of the condition and highlights some approaches that have disease-modifying effects in proof-of-concept studies.
Peripheral sensitization is the reduction in the threshold of excitability of sensory neurons that results in an augmented response to a given external stimulus. This poster outlines the excitatory and inhibitory signaling pathways involved in modulation of peripheral sensitization. The role of ion channels, GPCRs, neurotrophins, and cytokines in sensory neurons are also described.
Parkinson's disease (PD) causes chronic disability and is the second most common neurodegenerative condition. This poster outlines the neurobiology of the disease, as well as highlighting current therapeutic treatments for symptomatic PD, and emerging therapeutic strategies to delay PD onset and progression.