• Matija Boric, Antonia Jelicic Kadic, and Livia Puljak.
• Laboratory for Pain Research, University of Split School of Medicine, Soltanska 2, 21000 Split, Croatia. Electronic address: matija.boric@mefst.hr.
• Neurosci. Lett. 2014 Sep 5;579:151-6.

AbstractThe activation of calcium/calmodulin-dependent protein kinase II (CaMKII) has been proposed as a key factor in chronic pain development. This study therefore aimed to investigate the expression of CaMKII in the dorsal horn in a rat model of early phase diabetes mellitus (DM) types 1 and 2. Sprague-Dawley rats were used. DM1 was induced using streptozotocin (STZ) (55mg/kg injected intraperitoneally (i.p.)). DM2 was induced using a combination of a high fat diet (HFD) and STZ (35mg/kg i.p.). Controls received an i.p. injection of pure citrate buffer solution. DM2 animals and their controls also received HFD 2 weeks prior to the i.p. injection. Rats were sacrificed 2 weeks and 2 months after diabetes induction. The expression of tCaMKII, pCaMKIIα and IB4 in the dorsal horns was quantified using immunohistochemistry. Increased expression of tCaMKII and pCaMKIIα was seen in the dorsal horns of DM1 animals 2 weeks and 2 months after diabetes induction. In DM2 animals, similar changes in the expression of tCaMKII and pCaMKIIα were observed after 2 weeks, but not after 2 months. The expression of pCaMKIIα was most pronounced in laminae I-III. No difference in IB4 expression was observed between the groups. These results suggest a potential role for CaMKII in diabetic neuropathy development. Inhibition of CaMKII signaling pathways should be further explored as a potential treatment target in painful diabetic neuropathy.Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.

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