[Changes of intracellular calcium-regulating mechanisms of primary and secondary sensory neurones in periferal inflammation]. / Porushennia funktsii vnutrishn'oklitynnykh kal'tsiirehuliuiuchykh mekhanizmiv pervynnykh i vtorynnykh sensornykh neironiv pry peryferychnomu zapalenni.

Here we summarize the results of experimental investigation of changes in intracellular calcium homeostasis in mice and rat primary (dorsal root ganglia, DRG) and secondary (dorsal horn, DH) sensory neurons under carrageenan-induced periferal inflammation. A decrease in a calcium accumulation in both inositoltriphosphate- and caffeine-sensitive endoplasmic reticulum calcium stores has been detected in primary sensory neurons under condition of peripheral inflammation. We have also shown a decrease in the caffeine-induced calcium release in dorsal horn neurons of inflamed rat as compared to control ones. Decrease in the Ca2+ -accumulating properties of mitochondria has been demonstrated in both DRG and DH neurons with carrageenan-induced inflammation as compared with neurons of control animals. We conclude that changes in Ca2+ -regulating structures of primary and secondary sensory neurons could possibly lead to alterations in the transmission of nociceptive signals during inflammation.

[Changes in intracellular mechanisms in sensory neurons in experimental diabetes mellitus]. / Porushennia vnutrishn'oklitynnykh mekhanismiv sensornykh neironiv pry eksperymental'nomu tsukrovomu diabeti.

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.