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Calcium signalling in sensory neurones and peripheral glia in the context of diabetic neuropathies
Alexei Verkhratsky1, Paul Fernyhough2
1Faculty of Life Sciences, The University of Manchester, Manchester M13 9PT, UK; Achucarro Center for Neuroscience, IKERBASQUE, Basque Foundation for Science, 48011 Bilbao, Spain; University of Nizhny Novgorod, Nizhny Novgorod 603022, Russia; Kazan Federal University, Kazan 420111, Russia.
Abstract:
Peripheral sensory nervous system is comprised of neurones with their axons and neuroglia that includes satellite glial cells in sensory ganglia, myelinating, non-myelinating and perisynaptic Schwann cells. Pathogenesis of peripheral diabetic polyneuropathies is associated with aberrant function of both neurones and glia. Deregulated Ca(2+) homoeostasis and aberrant Ca(2+) signalling in neuronal and glial elements contributes to many forms of neuropathology and is fundamental to neurodegenerative diseases. In diabetes both neurones and glia experience metabolic stress and mitochondrial dysfunction which lead to deregulation of Ca(2+) homeostasis and Ca(2+) signalling, which in their turn lead to pathological cellular reactions contributing to development of diabetic neuropathies. Molecular cascades responsible for Ca(2+) homeostasis and signalling, therefore, can be regarded as potential therapeutic targets.
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