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J Neurophysiol (October 29, 2003). doi:10.1152/jn.00735.2003
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Submitted on July 31, 2003
Accepted on October 13, 2003

The Roles of CaMKII, PKA and PKC in the Induction and Maintenance of LTP of C-Fiber Evoked Field Potentials in Rat Spinal Dorsal Horn

Hong-Wei Yang1, Xiao-Dong Hu1, Hong-Mei Zhang1, Wen-Jun Xin1, Ming-Tao Li2, Tong Zhang1, Li-Jun Zhou1, and Xian-Guo Liu1*

1 Department of Physiology, Zhongshan Medical School of Sun Yat-sen University, Guangzhou, Guangdong, China
2 Department of Pharmacology, Zhongshan Medical School of Sun Yat-sen University, Guangzhou, Guangdong, China

* To whom correspondence should be addressed. E-mail: xgliu{at}gzsums.edu.cn.

Long-term potentiation (LTP) of C-fiber evoked field potentials in spinal dorsal horn may be relevant to hyperalgesia, an increased response to noxious stimulation. But the mechanism underlying this form of synaptic plasticity is still unclear. Considerable evidences have shown that calcium/calmodulin-dependent protein kinase II (CaMKII), protein kinase A (PKA) and protein kinase C (PKC) are important for LTP in hippocampus. In present work the roles of these three protein kinases in the induction and maintenance of LTP of C-fiber evoked field potentials were evaluated by application of specific inhibitors of CaMKII (KN-93 and AIP), PKA (Rp-CPT-cAMPS) and PKC (chelerythrine and Go 6983) at the recording segments before and after LTP induction in Urethane anesthetized Sprague-Dawley rats. We found (i) both KN-93 and AIP, when applied at 30 min prior to tetanic stimulation, completely blocked LTP induction. At 30 min after LTP induction KN-93 and AIP reversed LTP completely and at 60 min after LTP induction they depressed spinal LTP in most rats tested. Three hour after LTP induction, however, KN-93 or AIP did not affect the spinal LTP. (ii) Rp-CPT-cAMPS, chelerythrine or Go 6983 blocked the spinal LTP when applied at 30 min before tetanic stimulation and reversed LTP completely at 15 min after LTP induction. In contrast, at 30 min after LTP induction the drugs never affected the spinal LTP. These results suggest that activation of CaMKII, PKA and PKC may be crucial for the induction and the early-phase but not for the late-phase maintenance of the spinal LTP.




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