摘要

Abnormal neuronal calcium (Ca(2+)) homeostasis has been implicated in numerous diseases of the nervous system. The pathogenesis of two increasingly common disorders of the peripheral nervous system, namely neuropathic pain and diabetic polyneuropathy, has been associated with aberrant Ca(2+) channel expression and function. Here we review the current state of knowledge regarding the role of Ca(2+) dyshomeostasis and associated mitochondrial dysfunction in painful and diabetic neuropathies. The central impact of both alterations of Ca(2+) signalling at the plasma membrane and also intracellular Ca(2+) handling on sensory neurone function is discussed and related to abnormal endoplasmic reticulum performance. We also present new data highlighting sub-optimal axonal Ca(2+) signalling in diabetic neuropathy and discuss the putative role for this abnormality in the induction of axonal degeneration in peripheral neuropathies. The accumulating evidence implicating Ca(2+) dysregulation in both painful and degenerative neuropathies, along with recent advances in understanding of regional variations in Ca(2+) channel and pump structures, makes modulation of neuronal Ca(2+) handling an increasingly viable approach for therapeutic interventions against the painful and degenerative aspects of many peripheral neuropathies.

  • 出版日期2010-2