[Molecular neuropharmacology of nociceptive transmission and opioid receptors].
Kyoto, Japan. In Yakugaku Zasshi, 2000
Using cloned cDNA for OPRs, we demonstrated (1) the distribution of mRNAs for OPRs in the rat central nervous system, (2) coexistence of each type of mRNA for mu-, delta- and kappa-OPRs and pre-protachykinin A mRNA in the dorsal root ganglion neurons, (3) an increased expression of mu- and kappa-OPR mRNAs in the I-II layers of rat lumbar dorsal horn with an adjuvant arthritis in the hind limb, (4) the inhibitions of N- and Q-types of Ca2+ channels by mu- and kappa-OPR agonists and (5) cross-desensitization of the inhibition through a common intracellular phosphorylation-independent mechanism, (6) pharmacological characterization of "antagonist analgesics" as partial agonists at every type of OPRs, and (7) the key-structure(s) of OPRs for discriminative binding of DAMGO to mu-OPR.
[Mechanisms for the development of quinolone resistance].
In Nihon Rinsho, 1997
Bacterial resistance to the quinolones probably results from : 1) mutations with chromosomal genes of DNA gyrase or DNA topoisomerase in E. coli and S. aureus, 2) decreased permeability of the cell envelope through OmpF, porin-forming protein, in gram-negative bacteria, and 3) activation of active efflux-mediated permeability through the cell membrane protein, either NorA in S. aureus or Opr in P. aeruginosa.