Ion Channels of Nociception

Dear Colleagues,

Molecular mechanisms of pain - especially of neuropathic, migraine and cancer pain - remain largely unsolved. It is known that pain signals are typically initiated in the peripheral terminals of dorsal root or trigeminal ganglia neurons. These nerve terminals are equipped with specific receptors reacting to chemical or physical stimuli, as well as a range of specific voltage-gated ion channels contributing to generation and propagation of nociceptive spikes.

The molecular structures of many ion channels implicated in nociception are known, facilitating the development of new anti-nociceptive (analgesic) medicines. However, some new players in nociception have emerged only recently, for example mechanosensitive Piezo and the CRAC Orai1 channels. Moreover, the function of some ion channels, especially those which can counteract nociception, for instance, potassium K2P channels, is not well characterized. There are also gaps in understanding the role of ion channels in situ, ion channel interactions, functional role of sensitization-desensitization and ion channel inactivation, endogenous modulators and other important aspects of functioning of excitable nociceptive neurons and partnering non-excitable cells.

This Special Issue on 'Ion Channels of Nociception' aims to collect reviews and original papers devoted to elucidating the role of receptor- and voltage-gated ion channels in pain signaling. Together, these will shed light on the molecular mechanisms underlying the generation and propagation of nociceptive signals, supporting research into new pain therapies.

Prof. Dr. Rashid Giniatullin
Guest Editor

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