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Biological Activity for VU 10010
VU 10010 is a selective allosteric potentiator of M4 acetylcholine receptors (EC50 values are 33 and 0.7 nM for ACh in the absence and presence of VU10010 respectively). Binds to an allosteric site on the receptor increasing affinity for ACh and coupling to G-proteins.
Technical Data for VU 10010
|Storage||Store at +4°C|
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.
Solubility Data for VU 10010
|Solvent||Max Conc. mg/mL||Max Conc. mM|
Preparing Stock Solutions for VU 10010
The following data is based on the product molecular weight 345.85. 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||2.89 mL||14.46 mL||28.91 mL|
|5 mM||0.58 mL||2.89 mL||5.78 mL|
|10 mM||0.29 mL||1.45 mL||2.89 mL|
|50 mM||0.06 mL||0.29 mL||0.58 mL|
References for VU 10010
References are publications that support the biological activity of the product.
Shirey et al (2008) An allosteric potentiator of M4 mAChR modulates hippocampal synaptic transmission. Nat.Chem.Biol. 4 42 PMID: 18059262
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Keywords: VU 10010, VU 10010 supplier, Selective, allosteric, potentiator, M4, receptors, Muscarinic, Receptors, Acetylcholine, ACh, VU10010, PAM, 3141, Tocris Bioscience
1 Citation for VU 10010
Citations are publications that use Tocris products. Selected citations for VU 10010 include:
Bell et al (2015) Acetylcholine release in mouse hippocampal CA1 preferentially activates inhibitory-selective interneurons via α4β2* nicotinic receptor activation. PLoS One 9 115 PMID: 25918499
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Literature in this Area
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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.