NPEC-caged-dopamineCaged dopamine CAS# 1257326-23-0 |
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Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
Cas No. | 1257326-23-0 | SDF | Download SDF |
PubChem ID | 90488901 | Appearance | Powder |
Formula | C17H18N2O6 | M.Wt | 346.33 |
Type of Compound | N/A | Storage | Desiccate at -20°C |
Solubility | Soluble to 100 mM in 1eq. NaOH and to 100 mM in DMSO | ||
Chemical Name | 1-(2-nitrophenyl)ethyl N-[2-(3,4-dihydroxyphenyl)ethyl]carbamate | ||
SMILES | CC(C1=CC=CC=C1[N+](=O)[O-])OC(=O)NCCC2=CC(=C(C=C2)O)O | ||
Standard InChIKey | PDNNZLULXSQJGZ-UHFFFAOYSA-N | ||
Standard InChI | InChI=1S/C17H18N2O6/c1-11(13-4-2-3-5-14(13)19(23)24)25-17(22)18-9-8-12-6-7-15(20)16(21)10-12/h2-7,10-11,20-21H,8-9H2,1H3,(H,18,22) | ||
General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
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About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
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Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. |
Description | NPEC ((N)-1-(2-nitrophenyl)ethyl) caged version of dopamine; releases dopamine leading to D1 receptor activation upon UV light illumination (360 nm). Induces PKA activation and c-Fos expression in cortical and striatal neurons, with striatal neurons demonstrating a significantly greater detection and sensitivity to sub-second dopamine signals as compared to cortical neurons. |
NPEC-caged-dopamine Dilution Calculator
NPEC-caged-dopamine Molarity Calculator
1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
1 mM | 2.8874 mL | 14.4371 mL | 28.8742 mL | 57.7484 mL | 72.1855 mL |
5 mM | 0.5775 mL | 2.8874 mL | 5.7748 mL | 11.5497 mL | 14.4371 mL |
10 mM | 0.2887 mL | 1.4437 mL | 2.8874 mL | 5.7748 mL | 7.2185 mL |
50 mM | 0.0577 mL | 0.2887 mL | 0.5775 mL | 1.155 mL | 1.4437 mL |
100 mM | 0.0289 mL | 0.1444 mL | 0.2887 mL | 0.5775 mL | 0.7219 mL |
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations. |
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Striatal neurones have a specific ability to respond to phasic dopamine release.[Pubmed:23551948]
J Physiol. 2013 Jul 1;591(13):3197-214.
The cAMP/protein kinase A (PKA) signalling cascade is ubiquitous, and each step in this cascade involves enzymes that are expressed in multiple isoforms. We investigated the effects of this diversity on the integration of the pathway in the target cell by comparing prefrontal cortical neurones with striatal neurones which express a very specific set of signalling proteins. The prefrontal cortex and striatum both receive dopaminergic inputs and we analysed the dynamics of the cAMP/PKA signal triggered by dopamine D1 receptors in these two brain structures. Biosensor imaging in mouse brain slice preparations showed profound differences in the D1 response between pyramidal cortical neurones and striatal medium spiny neurones: the cAMP/PKA response was much stronger, faster and longer lasting in striatal neurones than in pyramidal cortical neurones. We identified three molecular determinants underlying these differences: different activities of phosphodiesterases, particularly those of type 4, which strongly damp the cAMP signal in the cortex but not in the striatum; stronger adenylyl cyclase activity in the striatum, generating responses with a faster onset than in the cortex; and DARPP-32, a phosphatase inhibitor which prolongs PKA action in the striatum. Striatal neurones were also highly responsive in terms of gene expression since a single sub-second dopamine stimulation is sufficient to trigger c-Fos expression in the striatum, but not in the cortex. Our data show how specific molecular elements of the cAMP/PKA signalling cascade selectively enable the principal striatal neurones to respond to brief dopamine stimuli, a critical process in incentive learning.