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A relatively potent and selective antagonist of group I metabotropic glutamate receptors (mGlu1a), having no effect on group II (mGlu2) or group III (mGlu4) receptors expressed individually in baby hamster kidney cells. Has no effect on ionotropic glutamate receptors. Centrally active following systemic administration in vivo.
|Storage||Store at RT|
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.
|Solvent||Max Conc. mg/mL||Max Conc. mM|
Preparing Stock Solutions
The following data is based on the product molecular weight 221.21. Batch specific molecular weights may vary from batch to batch due to the degree of hydration, which will affect the solvent volumes required to prepare stock solutions.
|Concentration / Solvent Volume / Mass||1 mg||5 mg||10 mg|
|1 mM||4.52 mL||22.6 mL||45.21 mL|
|5 mM||0.9 mL||4.52 mL||9.04 mL|
|10 mM||0.45 mL||2.26 mL||4.52 mL|
|50 mM||0.09 mL||0.45 mL||0.9 mL|
References are publications that support the biological activity of the product.
Moroni et al (1997) Pharmacological characterization of 1-aminoindan-1,5-dicarboxylic acid, a potent mGluR1 antagonist. J.Pharmacol.Exp.Ther. 281 721 PMID: 9152378
Nielsen et al (1997) Class I mGlu receptor antagonist 1-aminoindan-1,5-dicarboxylic acid blocks contextual but not cue conditioning in rats. Eur.J.Pharmacol. 326 105 PMID: 9196260
Pellicciari et al (1995) 1-Aminoindan-1,5-dicarboxylic acid: a novel antagonist at phospholipase C-linked metabotropic glutamate receptors. J.Med.Chem. 38 3717 PMID: 7562903
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Keywords: AIDA, AIDA supplier, Potent, selective, group, I, antagonist, Group, Receptors, mGlu1, mGlu5, mGluR1, mGluR5, Glutamate, Metabotropic, UPF523, UPF, 523, (Metabotropic), 0904, Tocris Bioscience
9 Citations for AIDA
Citations are publications that use Tocris products. Selected citations for AIDA include:
Pan et al (2004) Effects of the group I metabotropic glutamate receptor agonist, DHPG, and injection stress on striatal cell signaling in food-restricted and ad libitum fed rats. BMC Neurosci 5 50 PMID: 15579204
Ady et al (2014) Type 1 metabotropic glutamate receptors (mGlu1) trigger the gating of GluD2 δ glutamate receptors. J Neurosci 15 103 PMID: 24357660
Mahler et al (2014) Modafinil attenuates reinstatement of cocaine seeking: role for cystine-glutamate exchange and metabotropic glutamate receptors. Proc Natl Acad Sci U S A 19 49 PMID: 23017017
Yeckel et al (1999) Multiple forms of LTP in hippocampal CA3 neurons use a common postsynaptic mechanism. Nat Neurosci 2 625 PMID: 10404192
De-May and Ali (2013) Cell type-specific regulation of inhibition via cannabinoid type 1 receptors in rat neocortex. J Neurophysiol 109 216 PMID: 23054605
Shin et al (2008) Dendritic glutamate release produces autocrine activation of mGluR1 in cerebellar Purkinje cells. EMBO Rep 105 746 PMID: 18174329
Saitoh et al (2016) Glutamate signals through mGluR2 to control Schwann cell differentiation and proliferation Scientific Reports 6 29856 PMID: 27432639
Cassé et al (2012) Glutamate controls tPA recycling by astrocytes, which in turn influences glutamatergic signals. J Neurosci 32 5186 PMID: 22496564
Wibrand et al (2010) Differential regulation of mature and precursor microRNA expression by NMDA and metabotropic glutamate receptor activation during LTP in the adult dentate gyrus in vivo. Eur J Neurosci 31 636 PMID: 20384810
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Literature in this Area
Tocris offers the following scientific literature in this area to showcase our products. We invite you to request* your copy today!
*Please note that Tocris will only send literature to established scientific business / institute addresses.
The key feature of drug addiction is the inability to stop using a drug despite clear evidence of harm. This poster describes the brain circuits associated with addiction, and provides an overview of the main classes of addictive drugs and the neurotransmitter systems that they target.
Major depressive disorder is characterized by depressed mood and a loss of interest and/or pleasure. Updated in 2015 this poster highlights presynaptic and postsynaptic targets for the potential treatment of major depressive disorder, as well as outlining the pharmacology of currently approved antidepressant drugs.
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.
Huntington's Disease Poster
Huntington's disease (HD) is a monogenic neurodegenerative disorder, which is characterized by the prevalent loss of GABAergic medium spiny neurons (MSN) in the striatum. This poster summarizes the MSN intracellular signaling pathways implicated in the pathology of HD, as well as highlighting the use of iPSCs for HD modeling.
Learning & Memory Poster
Recognition memory enables us to make judgements about whether or not we have encountered a particular stimulus before. This poster outlines the cellular mechanisms underlying recognition memory and its links to long-term depression, as well as the use of pharmacological intervention to assess the role of neurotransmitters in recognition memory.
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.