Related Experiment Video
Updated: May 5, 2026
Assessment of Sarcoplasmic Reticulum Calcium Reserve and Intracellular Diastolic Calcium Removal in Isolated Ventricular Cardiomyocytes
Published on: September 18, 2017
Changes of calcium/calmodulin-dependent protein kinase II expression in dorsal root ganglia during maturation in
Lejla Ferhatovic1, Antonia Jelicic Kadic1, Matija Boric1
1Laboratory for Pain Research, University of Split School of Medicine, Split, Croatia.
Abstract:
Calcium/calmodulin-dependent protein kinase II (CaMKII) is considered one of the key intracellular signaling proteins for development of neuropathy. We analyzed the expression of total CaMKII (tCaMKII) and its alpha, beta, gamma and delta isoforms in dorsal root ganglia (DRG) in a rat model of Diabetes mellitus type I (DM1), 6 months and 1 year after diabetes induction. Diabetes was induced with streptozotocin and confirmed by measuring glucose levels and weight increase. Immunohistochemistry was performed for detection of tCaMKII and its isoforms in L4 and L5 DRGs. A significant decrease of CaMKII alpha and beta isoforms was noted 6 months after diabetes induction, while CaMKII gamma and delta were significantly decreased after 12 months in diabetic rats compared to controls. Analysis of neuronal subgroups based on the neuronal diameter revealed that the expression of alpha, beta and delta isoforms decreased only in small-diameter neurons. In conclusion, a significant decrease of specific CaMKII isoforms in small-diameter DRG neurons may suggest involvement of CaMKII alpha, beta and delta in the development of complex events responsible for the development of neuropathy in long-term diabetes during maturation. CaMKII is a part of the neuronal pathway that regulates the firing properties of excitable cells, especially neurons, and decreased CaMKII activity may be responsible for generation of aberrant signals, hyperalgesia and neuropathic pain.
Insights
Decreased expression of specific Calcium/calmodulin-dependent protein kinase II (CaMKII) isoforms in small neurons of the dorsal root ganglia may contribute to diabetic neuropathy development and pain.
Area of Science:
- Neuroscience
- Molecular Biology
- Endocrinology
Background:
- Diabetic neuropathy is a common complication of diabetes mellitus.
- Calcium/calmodulin-dependent protein kinase II (CaMKII) is implicated in neuronal function and disease.
- Understanding CaMKII's role in diabetic neuropathy is crucial for developing targeted therapies.
Purpose of the Study:
- To investigate the expression of CaMKII and its isoforms in dorsal root ganglia (DRG) of a rat model of type 1 diabetes.
- To determine if CaMKII changes are associated with the development of diabetic neuropathy.
Main Methods:
- Diabetes was induced in rats using streptozotocin.
- Immunohistochemistry was used to analyze total CaMKII (tCaMKII) and its alpha, beta, gamma, and delta isoforms in L4 and L5 DRGs at 6 and 12 months post-induction.
- Neuronal subgroups were analyzed based on neuronal diameter.
Main Results:
- A significant decrease in CaMKII alpha and beta isoforms was observed at 6 months.
- CaMKII gamma and delta isoforms significantly decreased at 12 months in diabetic rats compared to controls.
- The expression of alpha, beta, and delta isoforms decreased specifically in small-diameter neurons.
Conclusions:
- Specific CaMKII isoforms (alpha, beta, delta) are downregulated in small DRG neurons in long-term diabetes.
- This downregulation suggests a role for CaMKII in the pathogenesis of diabetic neuropathy.
- Reduced CaMKII activity may lead to aberrant neuronal signaling, hyperalgesia, and neuropathic pain.
More Related Videos
Related Concept Videos
01:16Calmodulin-dependent Signaling
The Ca2+-CaM complex does not have enzymatic activity by itself. Instead, the complex binds downstream target proteins, including membrane proteins or enzymes,...
01:24Type II Diabetes II: Pathophysiology
01:26Type I Diabetes II: Pathophysiology