|Product Name||Cat #||Size|
|STA-500||1 x 50 µg|
|STA-530||1 x 50 µg|
|STC-800||1 x 0.1 mg|
|STC-410||1 x 50 µg|
|STC-760||1 x 50 µg|
|C-150||1 x 30 µg|
|STC-751||1 x 50 µg|
|F-120||1 x 1 mg|
Mibefradil dihydrochloride hydrate
|M-150||1 x 1 mg|
ML 218 hydrochloride
|M-166||1 x 5 mg|
NNC 55-0396 dihydrochloride
|N-205||1 x 5 mg|
|RTS-500||1 x 25 µg|
|T-140||1 x 5 mg|
- Lyophilized Powder Lyophilized Powder
This product is freeze dried. All water molecules have been removed.
- Bioassay Tested Bioassay Tested
This antibody has undergone quality control and has been approved by our professional team.
Alomone Labs is pleased to offer the CaV Channel Blockers for Pain Research Explorer Kit (#EK-385). The Explorer Kit contains CaV channel blockers for pain research, ideal for screening purposes.
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.