Opioid-Induced Hyperalgesia and CaMKII alpha

Many of my backstories have featured Pain Researchers.  In several, I have featured use of our our i-Fect ™ Transfection Kit for enhancing the delivery of siRNA in vitro and in vivo to study the expression of genes invovled in Neuropathic and Nociceptive Pain.

I am excited to present a recent publication that includes use of this kit to study Opioid-Induced Hyperalgesia. In this study Dr. Zaijie Jim Wang and his team at University of Illiniois Chicago down regulate CaMKII alpa expression. Their data implicates, for the first time, an essential role of CaMKII alpha as a cellular mechanism leading to and maintaining opioid-induced hyperalgesia.

Yan Chen, Cheng Yang, and Zaijie Jim Wang. Ca2+/Calmodulin-Dependent Protein Kinase II Is Required for the Initiation and Maintenance of Opioid-Induced Hyperalgesia. The Journal of Neuroscience, January 6, 2010, 30(1):38-46; doi:10.1523/JNEUROSCI.4346-09.2010.

…KN93 and KN92 were administered intrathecally by percutaneous puncture through the L5-L6 intervertebral space, as described previously (Hylden and Wilcox, 1980; Chen et al., 2009). A lateral tail flick was considered as success of the intrathecal injection. To inhibit CaMKII, CaMKII was targeted by small interfering RNA (siRNA). Four days after morphine pellet implantation, mice were treated with CaMKII siRNA (5′-CACCACCAUUGAGGACGAAdTdT-3′, 3′-dTdTGUGGUGGUAACUCCUGCUU-5′) (Zayzafoon et al., 2005) or Stealth RNAi negative control (Invitrogen) (2 µg, i.t., twice per day for 3 consecutive days). These oligos were mixed with the transfection reagent i-Fect (Neuromics), in a ratio of 1:5 (w/v) (Luo et al., 2005). Mechanical and thermal sensitivity tests were performed daily…