CaV Channel Antibodies for Pain Research Explorer Kit

A Screening Package of CaV Channel Antibodies for Pain Research Economically Priced
  • Lyophilized Powder
  • Antigen Incl.
Cat #: AK-360
Last update: 24/01/2020

Alomone Labs is pleased to offer the CaV Channel Antibodies for Pain Research Explorer Kit (#AK-360). This Explorer Kit includes CaV 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


Product NameCat #Size
Anti-CACNA1A (CaV2.1) Antibody
ACC-001 1 x 50 µl
Anti-CACNA1B (CaV2.2) Antibody
ACC-002 1 x 50 µl
Anti-CaV2.3 (CACNA1E) Antibody
ACC-006 1 x 50 µl
Anti-CACNA1G (CaV3.1) Antibody
ACC-021 1 x 50 µl
Anti-CaV3.2 (CACNA1H) Antibody
ACC-025 1 x 50 µl
Anti-CaV3.3 (CACNA1I) Antibody
ACC-009 1 x 50 µl

Scientific Background

Scientific Background
    • Voltage gated calcium channels (CaV) are key signal transducers that convert depolarization of the cell membrane into an influx of extracellular calcium ions. This ion influx mediates a wide range of critical intracellular processes since calcium is a second messenger that triggers muscle contraction, hormone and neurotransmitter release, regulation of enzymatic activities and altered patterns of gene expression. It is hypothesized that channels regulating the influx of ionized calcium may be particularly important in regulating system excitability following nerve injury. Myelinated and unmyelinated sensory axons contain CaV1.2. In the dorsal horn, L-type calcium channels are predominantly located on neuronal soma and dendrites. Spinal motoneurons also express both CaV1.2 and CaV1.3. Following nerve resection there is a downregulation of various CaV subunits. These observations suggest that nerve injury, meaning induced reduction of CaV1-type mRNAs may contribute to increased spontaneous excitability of damaged neurons. This is also supported by observation that axotomy-induced excitability is associated with a decrease in the calcium-dependent potassium currents that are secondary to decreased Ca2+ influx. Another type of calcium channels involved in pain mediation are N-type channels. These channels are located in the dorsal root ganglia and in the superficial dorsal horn, especially in laminae I and II of the superficial dorsal horn, where nociceptive primary afferents synapse.  Electrophysiology studies emphasize those small DRG cells, which contain and release a variety of neuropeptides such as substance P and CGRP, express N-type calcium currents. In humans, N-type blockers such as Ziconotide have a potent anti-allodynic effect in a variety of complex pain states arising from nerve injury.
Shipping and Ordering information