Voltage Gated Sodium Channel Assays
Background of Voltage Gated Sodium Channel
Formed by the membrane main protein, voltage-gated sodium channels (NaV) are responsible for the generation of Na+ currents in multiple cell types, such as nerve, muscle, and neuroendocrine cells. There are three main states of Nav channels, including the closed quiescent state, the open conducting state, as well as the non-conducting inactive state. The Nav channels have served as an important class of drug targets against pain and other pathology conditions.
Fig.1. Diagram of a voltage-sensitive sodium channel.
Distribution of Voltage Gated Sodium Channel
Nav1.1, Nav1.2, and Nav1.3 subtypes are expressed in the central nervous system (CNS), while Nav1.4 and Nav1.5 channels are abundant in skeletal and cardiac muscles, respectively. Nav1.6 can be expressed in both the peripheral and central nervous system, whereas the expression of Nav1.7, Nav1.8, and Nav1.9 can be detected in the peripheral nervous system (PNS).
Diversity and Functions of Voltage Gated Sodium Channel
In general, the voltage-gated sodium channels contain one alpha subunit to form the ion conduction pore and one to two beta subunits with multiple functions. The alpha subunits are named NaV1.1 through Nav1.9, while the beta subunits contain SCN1B, SCN2B, SCN3B, and SCN4B.
| Types | Gene | Associated human channelopathies | Activators | Blockers |
| NaV1.1 | SCN1A |
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| NaV1.2 | SCN2A |
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| NaV1.3 | SCN3A |
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| NaV1.4 | SCN4A |
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| NaV1.5 | SCN5A |
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| NaV1.6 | SCN8A |
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| NaV1.7 | SCN9A |
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| NaV1.8 | SCN10A |
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| NaV1.9 | SCN11A |
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| β1 | SCN1B |
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| β2 | SCN2B |
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| β3 | SCN3B |
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| β4 | SCN4B |
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Assay List of Voltage Gated Sodium Channel
Creative Biolabs can provide a range of assays of voltage gated sodium channels. You can choose the assay in the list or contact us for more information:
Published Data
| Paper Title | The Role of Voltage-Gated Sodium Channels in Pain Signaling |
| Journal | Physiological reviews |
| Published | 2019 |
| Abstract | Acute pain signaling is highly evolutionarily conserved. In contrast, chronic pain is caused by injury and disease and is related to the sensitivity of the somatosensory nervous system. It has been shown in the literature that the voltage-gated sodium channel (VGSC) is an important determinant of the excitability of sensory neurons and is involved in processes including the initial transduction of sensory stimuli, the electrical generation of action potentials, and the release of neurotransmitters from sensory neuron terminals. Furthermore, changes in VGSC expression levels as well as post-translational modifications contribute to the sensitization of sensory neurons in chronic pain states. Nav1.1, Nav1.6, Nav1.7, Nav1.8, and Nav1.9 are all expressed by adult sensory neurons. Among them, gene mutations of Nav1.7, Nav1.8, and Nav1.9 have been confirmed to be associated with pain disorders. These findings will have implications for the development of new analgesics. |
| Result |
Based on the current advanced gene sequencing technology and bioinformatics analysis, we have a deeper understanding of Mendelian pain disorders. Mutations in Nav1.7, 1.8, and 1.9 have been detected in related diseases. This provides important information for studying the normal function and pathophysiological role of ion channels. The advance applies to rare Mendelian pain disorders as well as common acquired neuropathic pain states. This can fundamentally change outcomes at the cellular and system level.
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Fig.2. Voltage-gated sodium channel structure. (Bennett, et al., 2019)
Reference
- Bennett, D.L.; et al. The role of voltage-gated sodium channels in pain signaling. Physiological reviews. 2019, 99(2): 1079-1151.
