Ion channels in somatosensory transmission: an introduction to the collection

Editorial

Peripheral somatosensory neurons underlie a variety of somatic sensations, which can be torturing or pleasant. These neurons are different from most other neurons in the mammalian nervous system in several key features. Thus, these neurons have a very specific anatomy, being pseudo-unipolar neurons with a single giant neuritis that are split in a t-way and can reach several meters in length in some mammals. The action potentials in the somatosensory neurons normally originate not at the axon initial segment (as in most CNS neurons) but at the nerve endings within the peripheral tissues (skin, muscles, joints, blood vessels, internal organs etc.); therefore, the giant neurites (or fibres) of the somatosensory neurons serve both axonic and dendritic functions. Major segments of a somatosensory neuron (that is the cell body, axonal stem, peripheral and most of the central branches of the fibre) are located outside the blood-brain barrier and, thus, are exposed to circulation at least to some extent. Yet, the central branch of the fiber enters the CNS as it synapses in the dorsal horn of the spinal cord. Thus, the peripheral somatosensory neuron in fact belongs to both peripheral and central nervous systems simultaneously. There are other important distinctions of peripheral somatosensory neurons, for instance they accumulate high intracellular chloride levels so that, in contrast to the CNS neurons, activation of chloride channels in these neurons can result in excitation instead of inhibition (Liu et al., 2010). Finally, these neurons express a specific set of ion channels, some of which are more or less unique to this type of neurons (Raouf et al., 2010), such as a voltage gated Na⁺ channel Nav1.7 for example.

Recent decades have seen a tremendous advance in our understanding of mechanisms of peripheral sensory neuron excitability and how these are different from CNS neurons; specific subpopulations of sensory neurons that respond to particular stimuli (e.g. mechanical, thermal, chemical) and underlie specific sensations (e.g. touch, pain, itch) have been identified (Basbaum et al., 2009); many sensory neuron-specific ion channels have been cloned and characterised (Raouf et al., 2010); and mechanisms of many sensory dysfunctions, leading, for instance, to chronic pains have been revealed (McMahon et al., 2006). Yet, new channels are being cloned and new mechanisms are being characterized every year and there is still huge uncharted territory to discover. Thus, despite the cloning of Piezo channels (Coste et al., 2010), the molecular mechanisms of mechanotrasduction are still not completely understood; mechanisms behind many basic phenomena such as noxious cold sensation or inflammatory hyperalgesia are intensely debated. Most importantly, despite decades of research and investment, there is still little progress in analgesic drug development and opioids are still a gold standard.

This F1000Research article collection is focused on the current advances in understanding function and regulation of ion channels controlling excitability and synaptic transmission within somatosensory pathways. The focus is on the peripheral neurons but studies of central mechanisms that integrate peripheral inputs are also welcome. We also welcome discussions of emerging approaches, methods and techniques in somatosensory physiology.