Overview
Cat #: AK-365_KIT
Size: 28 Vials
Form: Lyophilized
Alomone Labs is pleased to offer the NaV Channel Antibodies for Pain Research Explorer Kit (#AK-365). This Explorer Kit includes NaV Channel antibodies for Pain Research with their respective peptide control antigen. An ideal tool for screening purposes.
For research purposes only, not for human use
Compounds
Scientific Background
Scientific Background Voltage dependent sodium channels (NaV) have functions in most electrically active cells and are vital for the propagation of action potential in most cells. NaV channel inhibiting drugs have been long used as analgesic drugs with relatively mild side effects and a safe pharmacological profile. The mechanism of analgesia by NaV channel blockage has been extensively studied. Four NaV channel subtypes involved in pain- NaV1.3, 1.7, 1.8 and 1.9. Nav1.8 and 1.9 are referred to as tetrodotoxin (TTX)-resistant channels and are implicated in pain relief because action potentials in nociceptive neurons are characteristically also resistant to TTX. The relatively depolarized voltage dependence of inactivation of NaV1.8 also allows these channels to contribute to action potential generation even at depolarized membrane potentials as may occur following nerve injury or pain signaling. Importantly, NaV1.8 was found to be almost exclusively localized to nociceptive DRG neurons – mainly in small diameter unmyelinated C-fibers, but also in some medium diameter, thinly myelinated Aδ-fibers. NaV1.9 channels are exclusively expressed in C-fibers. Studies suggest that it is responsible for the persistent component of TTX-r currents that are found in nociceptive DRG neurons, having very slow kinetics and a large window current due to a hyperpolarised voltage dependence of activation compared to inactivation. NaV1.9 knockout mice have no neuropathic pain phenotype, but do show reduced hypersensitivity to inflammatory stimuli. NaV1.7 is also expressed in DRG cells, but unlike NaV1.8 and 1.9, it is sensitive to TTX and is expressed in both nociceptive and non-nociceptive peripheral neurons. NaV1.7 channels have unusually slow kinetics of open-state and closed-state inactivation, and these unusual gating properties may allow the channels to stay open during slow depolarizations, thus amplifying pain signals.
References
- Clare, J.J. (2010) Expert Opin. Investig. Drugs 19, 45.
