Calcium signal prolongation in sensory neurones of mice with experimental diabetes

Elena Kostyuk, Nina Pronchuk, Anatoly Shmigol

Research output: Contribution to journalArticlepeer-review

57 Citations (Scopus)

Abstract

Depolarization-induced Ca2+ transients were studied in dorsal root ganglion neurones of different size (large, 30–45 μ m; small, 18–25 μ m in diameter) from normal and diabetic mice. Whereas in large neurones no definite changes in the amplitude and time course of the transients were observed, in small neurones the decay of transient became substantially prolonged during streptozotocin-induced and spontaneously occurring diabetes. As small and large neurones differ substantially in their mechanisms of Ca2+transient termination, we conclude that the prolongation of Ca2+transients, probably induced by chronic hyperglycaemia, is specific only for small sensory neurones (transmitting mostly nociceptive signals) and may be a cause of the increased pain sensitivity often accompanying this disease.

Original languageEnglish
Pages (from-to)1010-1012
Number of pages3
JournalNeuroReport
Volume6
Issue number7
DOIs
Publication statusPublished - May 1995
Externally publishedYes

Keywords

  • Caffeine-sensitive calcium stores
  • Cytoplasmic calcium
  • Experimental diabetes
  • Sensory neurones

ASJC Scopus subject areas

  • Neuroscience(all)

Fingerprint

Dive into the research topics of 'Calcium signal prolongation in sensory neurones of mice with experimental diabetes'. Together they form a unique fingerprint.

Cite this