[Changes in intracellular mechanisms in sensory neurons in experimental diabetes mellitus]

Here we summarises the results of experimental investigation of changes in intracellular calcium homeostasis in sensory neurones of rats with streptozotocin-induced diabetes mellitus. Decrease in the calcium-accumulating function of both inositol-trisphosphate- as well as caffeine-sensitive endoplasmic reticulum has been detected both in primary sensory neurones of dorsal root ganglia and in secondary neurones of the spinal cord dorsal horn. Predominant depression in the functioning of metabotropic receptors of ligand-gated channels compared with those of ionotropic ones has been demonstrated. Changes in the pharmacological sensitivity of potential-operated calcium channels (predominantly of L-type), linked, probably, with alterations of functional connections between membrane channels and endoplasmic reticulum, are described. A predominant role of changes in the functioning of intracellular Ca(2+)-accumulating structures, leading to prolongation of depolarisation-induced Ca2+ transients in primary and secondary sensory neurones and corresponding changes in the transmission of nociceptive signals during diabetic neuropathy are discussed.