Calcium signalling in sensory neurones and peripheral glia in the context of diabetic neuropathies

• Pathogenesis of peripheral diabetic polyneuropathies is associated with aberrant function of both neurones and glia.
• Deregulation of Ca2+ homeostasis in neurones and glia contribute to development of diabetic neuropathies.
• Molecular cascades responsible for Ca2+ homeostasis and signalling can be regarded as potential therapeutic targets.

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 Ca2+ homoeostasis and aberrant Ca2+ 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 Ca2+ homeostasis and Ca2+ signalling, which in their turn lead to pathological cellular reactions contributing to development of diabetic neuropathies. Molecular cascades responsible for Ca2+ homeostasis and signalling, therefore, can be regarded as potential therapeutic targets.