ACUPUNCTURE AND MORPHINE ANALGESIA INHIBITORY SYSTEMS AND ITS CORRELATION WITH MORPHINE TOLERANCE

Author(s):  
C. Takeshige ◽  
M. Kobori ◽  
H. Mera
Pain ◽  
2005 ◽  
Vol 115 (1) ◽  
pp. 50-59 ◽  
Author(s):  
Yehuda Shavit ◽  
Gilly Wolf ◽  
Inbal Goshen ◽  
Dina Livshits ◽  
Raz Yirmiya

2006 ◽  
Vol 291 (2) ◽  
pp. R315-R326 ◽  
Author(s):  
Camron D. Bryant ◽  
Shoshana Eitan ◽  
Kevin Sinchak ◽  
Michael S. Fanselow ◽  
Christopher J. Evans

Multiple studies demonstrate that coadministration of N-methyl-d-aspartate (NMDA) receptor antagonists with the opioid agonist morphine attenuates the development of analgesic tolerance. Sex differences in the effects of noncompetitive, but not competitive NMDA receptor antagonists on acute morphine analgesia, have been reported in mice, yet the role of sex in modulation of morphine tolerance by NMDA receptor antagonists has yet to be addressed. Therefore, we tested whether there is a sex difference in the effect of NMDA receptor antagonists on the development of morphine analgesic tolerance in C57BL/6J mice. Acutely, at a dose required to affect morphine tolerance in male mice, the noncompetitive NMDA receptor antagonist dizocilpine (MK-801) prolonged morphine analgesia similarly in both sexes in the hot plate and tail withdrawal assays. In the hot plate assay, coadministration of MK-801 or the competitive antagonist 3-(2-carboxpiperazin-4-yl)propyl-1-phosphanoic acid (CPP) with morphine attenuated the development of tolerance in male mice, while having no effect in females. Like normal and sham females, ovariectomized mice were similarly insensitive to the attenuation of morphine tolerance by MK-801 in the hot plate assay. Surprisingly, in the tail withdrawal assay, MK-801 facilitated the development of morphine-induced hyperalgesia and tolerance in males but not females. The results demonstrate that male mice are more sensitive to modulation of nociception and morphine analgesia after repeated coadministration of NMDA receptor antagonists. Furthermore, the underlying mechanisms are likely to be different from those mediating the sex difference in the modulation of acute morphine analgesia that has previously been reported.


2004 ◽  
Vol 20 (12) ◽  
pp. 3516-3519 ◽  
Author(s):  
Kazuaki Yokoyama ◽  
Takashi Kurihara ◽  
Hironao Saegusa ◽  
Shuqin Zong ◽  
Koshi Makita ◽  
...  

1990 ◽  
Vol 176 (1) ◽  
pp. 35-44 ◽  
Author(s):  
C.T. Dourish ◽  
M.F. O'Neill ◽  
J. Coughlan ◽  
S.J. Kitchener ◽  
D. Hawley ◽  
...  

2011 ◽  
Vol 115 (6) ◽  
pp. 1261-1270 ◽  
Author(s):  
Chengshui Zhao ◽  
Michael Leitges ◽  
Robert W. Gereau

Background Protein kinase C (PKC) is a family of serine/threonine kinases that contains more than 10 isozymes. Evidence suggests that PKC may play important roles in pain modulation, but the isozyme-specific effects of PKC on different aspects of pain modulation are not fully understood. We hypothesize that different PKC isozymes play different roles in different aspects of pain modulation. Methods The nociceptive behaviors of mice with deletion of PKCα, β, γ, or δ in multiple pain models were compared with their respective wild-type littermates. Also, morphine analgesia and the development of morphine tolerance in mice with deletion of PKCγ were compared with their respective wild-type littermates. Results Thermal hyperalgesia induced by complete Freund's adjuvant injection was significantly attenuated by the deletion of PKCβ, γ, or δ, but not PKCα. Deletion of PKCγ significantly attenuated neuropathic mechanical allodynia induced by spared nerve injury, whereas deletion of PKCα enhanced this allodynia. Baseline thermal and mechanical sensitivity, nociceptive behaviors induced by formalin, mechanical allodynia induced by complete Freund's adjuvant injection, were not altered by deletion of PKCα, β, γ, or δ. Finally, morphine analgesia and the development of morphine tolerance were not altered in PKCγ-deficient mice. Conclusions PKC has isozyme-specific effects in pain modulation.


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