There is a large variety of K1 channels66 and their significance in pain signaling is far from understood. Classic voltage-gated K1 channels, often called delayed rectifiers, have six transmembrane domains and can be divided into nine gene subfamilies. The KV1 subfamily is the most explored among subtypes of sensory neurons.67 KV1.1 and KV1.2 are present in large-diameter sensory neurons, whereas KV1.4 is present in most small sensory neurons that express NaV1.8, making it the candidate nociceptive delayed rectifier. The activation of voltage-gated K1 channels ultimately decreases the excitability of a cell. Thus, K1 channels are prime molecular targets for suppressing hyperactive neurons, and might, therefore, prove useful in suppressing hypersensitivity.
Other K1 channels that figure prominently in excitation of neurons, are the M channel (KCNQ gene), the H channel- (HCN gene) and calcium-activated K channels. All these channels are thought to be present on some populations of sensory neurons.68,69,70 However, their relevance to pain is largely unknown.
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