| First Author | Niikura K | Year | 2008 |
| Journal | Neurosci Lett | Volume | 433 |
| Issue | 1 | Pages | 54-8 |
| PubMed ID | 18262361 | Mgi Jnum | J:136577 |
| Mgi Id | MGI:3796502 | Doi | 10.1016/j.neulet.2007.12.042 |
| Citation | Niikura K, et al. (2008) Implication of endogenous beta-endorphin in the inhibition of the morphine-induced rewarding effect by the direct activation of spinal protein kinase C in mice. Neurosci Lett 433(1):54-8 |
| abstractText | It has often been proposed that opioid addiction does not arise as a consequence of opioid treatment for pain. Recently, we demonstrated that activated protein kinase C (PKC) in the spinal cord associated with chronic pain-like hyperalgesia suppressed the morphine-induced rewarding effect in mice. In the present study, we investigated whether a gene deletion for an endogenous mu-opioid peptide beta-endorphin could affect pain-like behavior and the suppression of the morphine-induced rewarding effect by the direct activation of PKC in the spinal cord. We found that activation of spinal PKC by intrathecal (i.t.) treatment with phorbol 12,13-dibutyrate (PDBu), a specific PKC activator, caused thermal hyperalgesia, pain-like behaviors and suppression of the morphine-induced rewarding effect. This suppression of morphine reward was eliminated in mice that lacked beta-endorphin. In contrast, thermal hyperalgesia and pain-like behaviors were not affected in beta-endorphin knockout mice. These results suggest that the activation of PKC in the spinal cord may play an essential role in the suppression of the morphine-induced rewarding effect in mice with neuropathic pain through the constant release of beta-endorphin. |
