High affinity neuronal nicotinic ACh receptor partial agonist (Ki values are 0.058, 0.26 and 7.2 μM for rat α7, rat α4β2 and fish skeletal muscle nAChRs respectively). Also stimulates Ca2+-dependent catecholamine release from rat adrenomedullary cells in vitro.
|Storage||Desiccate at RT|
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
All Tocris products are intended for laboratory research use only.
|Solvent||Max Conc. mg/mL||Max Conc. mM|
Preparing Stock Solutions
The following data is based on the product molecular weight 198.69. Batch specific molecular weights may vary from batch to batch due to solvent 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||5.03 mL||25.16 mL||50.33 mL|
|5 mM||1.01 mL||5.03 mL||10.07 mL|
|10 mM||0.5 mL||2.52 mL||5.03 mL|
|50 mM||0.1 mL||0.5 mL||1.01 mL|
References are publications that support the products' biological activity.
Kem et al (1997) Anabaseine is a potent agonist on muscle and neuronal alpha-bungarotoxin-sensitive nicotinic receptors. J.Pharmacol.Exp.Ther. 283 979 PMID: 9399967
Parker et al (1998) Neuronal nicotinic receptor β2 and β4 subunits confer large differences in agonist binding affinity. Mol.Pharmacol. 54 1132 PMID: 9855644
Lu et al (1999) Desensitization of nicotinic agonist-induced [3H]γ-aminobutyric acid release from mouse brain synaptosomes is produced by subactivating concentrations of agonists. J.Pharmacol.Exp.Ther. 291 1127 PMID: 10565833
Hong et al (2007) Effect of anabasine on catecholamine secreation from the perfused rat adrenal medulla. J.Cardiol. 50 351 PMID: 18186309
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Keywords: (+)-Anabasine hydrochloride, supplier, Neuronal, nicotinic, receptor, agonists, Acetylcholine, Receptors, Non-Selective, Subtypes, nAChR, Nicotinic, Receptors, (Non-selective), Nicotinic, Receptors, (Non-selective), Tocris Bioscience
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Literature in this Area
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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.