• Matija Boric, Antonia Jelicic Kadic, Lejla Ferhatovic, Damir Sapunar, and Livia Puljak.
• Laboratory for Pain Research, School of Medicine, University of Split, Split, Croatia.
• Neuroreport. 2013 Dec 4;24(17):992-6.

AbstractThe aim of this study was to investigate the expression of total calcium/calmodulin-dependent protein kinase II (CaMKII) and its phosphorylated α isoform in the dorsal horn of the spinal cord in an animal model of long-term diabetes. Diabetes was induced in Sprague-Dawley rats using 55 mg/kg streptozotocin, and expression of total CaMKII, the phosphorylated α-CaMKII isoform, and isolectin B4 was analyzed by immunohistochemical analysis in the dorsal horn of the spinal cord 6 and 12 months after diabetes induction. Results were compared with those for control rats of the same age. Increased expression of total CaMKII and its activated α isoform was seen in the dorsal horn of diabetic rats 6 months after diabetes induction. The increase in CaMKII fluorescence was restored to control values after 12 months. The expression of activated α-CaMKII 12 months after diabetes induction was most pronounced in laminae I-VI of the dorsal horn, not corresponding with the highest expression of isolectin B4 in laminae I-III. Increased expression of CaMKII in the dorsal horn during long-term diabetes could be involved in the development of neuropathic symptoms in diabetes. The expression pattern of CaMKII during long-term diabetes indicates that it affects the entire sensory input.

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