|Product Name||Cat #||Size|
Anti-Nicotinic Acetylcholine Receptor α6 (CHRNA6) (extracellular) Antibody
|ANC-006||1 x 50 µl|
Anti-Nicotinic Acetylcholine Receptor α7 (CHRNA7) (extracellular) Antibody
|ANC-007||1 x 50 µl|
Anti-Nicotinic Acetylcholine Receptor α9 (CHRNA9) Antibody
|ANC-019||1 x 50 µl|
Anti-Nicotinic Acetylcholine Receptor β4 (CHRNB4) (extracellular) Antibody
|ANC-014||1 x 50 µl|
- Lyophilized Powder Lyophilized Powder
This product is freeze dried. All water molecules have been removed.
- Antigen Incl. Control Antigen Included
This antibody is shipped with its antigen FREE of charge!
Alomone Labs is pleased to offer the nAChR Antibodies for Pain Research Explorer Kit (#AK-375). This Explorer Kit includes nAChR antibodies for pain research with their respective peptide control antigen. An ideal tool for screening purposes.
- Neuronal nicotinic acetylcholine receptors (nAChRs) are pentameric ligand-gated ion channels that exist as homomeric or heteromeric complexes of α and β subunits. To date, 12 neuronal subunits (α2–α10 and β2–β4) have been identified in mammals. Antinociceptive effects of nicotine, a relatively nonselective nAChR agonist, have been demonstrated in preclinical and clinical studies and evidence suggests that nicotine antinociception is mediated at least in part by α4β2 and/or α6β2. In addition, the α7 nAChR subtype may also contribute to antinociceptive effects of nicotine or other nAChR agonists. The α5 subunit is also involved in pain mediation but unlike other subunits it cannot form a functional homomeric receptor and must be expressed with either β2 or β41. Binding sites for nAChR ligands have been found in regions that control pain perception such as dorsal root ganglia, medullary nuclei and spinal cord dorsal horn. Acute noxious stimulation increases CSF levels while the increase of nAChR inhibitors in CSF fluid causes analgesia which suggests that the receptor is also involved in pain relief. In addition, nAChR receptors are also involved in tonic pain stimulation. Interestingly, inhibition of nAChR before injecting an agonist such as formalin results in an increase in pain behavior in rats rather than analgesia suggesting that the receptor has opposite roles in acute and chronic pain modulation2.