Faculty Collaboration Database

Differential expression of CaMKII isoforms and overall kinase activity in rat dorsal root ganglia after injury. Neuroscience 2015 Aug 06;300:116-27

Date

05/20/2015

Pubmed ID

25982557

Pubmed Central ID

PMC4485599

DOI

10.1016/j.neuroscience.2015.05.007

Scopus ID

2-s2.0-84930226027 (requires institutional sign-in at Scopus site)   19 Citations

Abstract

Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) decodes neuronal activity by translating cytoplasmic Ca(2+) signals into kinase activity that regulates neuronal functions including excitability, gene expression, and synaptic transmission. Four genes lead to developmental and differential expression of CaMKII isoforms (α, β, γ, δ). We determined mRNA levels of these isoforms in the dorsal root ganglia (DRG) of adult rats with and without nerve injury in order to determine if differential expression of CaMKII isoforms may contribute to functional differences that follow injury. DRG neurons express mRNA for all four isoforms, and the relative abundance of CaMKII isoforms was γ>α>β=δ, based on the CT values. Following ligation of the 5th lumbar (L5) spinal nerve (SNL), the β isoform did not change, but mRNA levels of both the γ and α isoforms were reduced in the directly injured L5 neurons, and the α isoform was reduced in L4 neurons, compared to their contemporary controls. In contrast, expression of the δ isoform mRNA increased in L5 neurons. CaMKII protein decreased following nerve injury in both L4 and L5 populations. Total CaMKII activity measured under saturating Ca(2+)/CaM conditions was decreased in both L4 and L5 populations, while autonomous CaMKII activity determined in the absence of Ca(2+) was selectively reduced in axotomized L5 neurons 21days after injury. Thus, loss of CaMKII signaling in sensory neurons after peripheral nerve injury may contribute to neuronal dysfunction and pain.

Author List

Bangaru ML, Meng J, Kaiser DJ, Yu H, Fischer G, Hogan QH, Hudmon A

Authors

Quinn H. Hogan MD Professor in the Anesthesiology department at Medical College of Wisconsin
Hongwei Yu MD Professor in the Anesthesiology department at Medical College of Wisconsin

MESH terms used to index this publication - Major topics in bold

Animals
Axotomy
Calcium-Calmodulin-Dependent Protein Kinase Type 2
Catalysis
Disease Models, Animal
Ganglia, Spinal
Gene Expression
HEK293 Cells
Humans
Hyperalgesia
Isoenzymes
Lumbar Vertebrae
Male
RNA, Messenger
Rats, Sprague-Dawley
Sensory Receptor Cells
Spinal Nerves