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International Journal of Endocrinology
Volume 2013, Article ID 532850, 11 pages
Research Article

Calcium Activity of Upper Thoracic Dorsal Root Ganglion Neurons in Zucker Diabetic Fatty Rats

1Department of Drug Design and Pharmacology, Faculty of Health and Medical Sciences, University of Copenhagen, 2100 Copenhagen, Denmark
2Non-Clinical Development, Novo Nordisk A/S, 2760 Maaloev, Denmark

Received 14 December 2012; Revised 19 February 2013; Accepted 20 February 2013

Academic Editor: Gunnar Gislason

Copyright © 2013 Marie Louise Ghorbani et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


The aim of the present study was to examine the calcium activity of C8-T5 dorsal root ganglion (DRG) neurons from Zucker diabetic fatty rats. In total, 8 diabetic ZDF fatty animals and 8 age-matched control ZDF lean rats were employed in the study. C8-T5 dorsal root ganglia were isolated bilaterally from 14 to 18 weeks old rats, and a primary culture was prepared. Calcium activity was measured ratiometrically using the fluorescent Ca2+-indicator Fura-2 acetoxymethyl ester. All neurons were stimulated twice with 20 mM K+, followed by stimulation with either 0.3 or 0.5 μM Capsaicin, alone or in combination with algogenic chemicals (bradykinin, serotonin, prostaglandin E2 (all 10−5 M), and adenosine (10−3 M)) at pH 7.4 and 6.0. Neurons from diabetic animals exhibited an overall increased response to stimulation with 20 mM K+ compared to neurons from control. Stimulation with Capsaicin alone caused an augmented response in neurons from diabetic animals compared to control animals. When stimulated with a combination of Capsaicin and algogenic chemicals, no differences between the two groups of neurons were measured, neither at pH 7.4 nor 6.0. In conclusion, diabetes-induced alterations in calcium activity of the DRG neurons were found, potentially indicating altered neuronal responses during myocardial ischemia.