![[Feedback]](/icons/banner/feedbackACT.gif){kind=icon}
![[For Subscribers]](/icons/banner/subscriberACT.gif){kind=icon}
![[Archive]](/icons/banner/archiveACT.gif){kind=icon}
![[Search]](/icons/banner/searchACT.gif){kind=icon}
![[Contents]](/icons/banner/tocACT.gif){kind=icon}
|
|
|
|
|
||
Vol. 57, Issue 1, 108-115, January 2000
i- and Inositol
Trisphosphate-Mediated Ca2+ Influx
Department of Molecular Pharmacology and Neuroscience, Nagasaki
University School of Pharmaceutical Sciences, Nagasaki, Japan
Kyotorphin is a dipeptidic neuropeptide (tyrosine-arginine) that has
specific receptor coupled to Gi and phospholipase C and elicits Met-enkephalin release. Here, we attempted to demonstrate the
in vivo evidence for the presynaptic mechanism by analyzing its
nociceptive responses after peripheral application. Kyotorphin elicited
potent nociceptive flexor responses at extremely low doses between 0.1 and 100 fmol after the intraplantar injection into the hind-limb of
mice. The site of action of kyotorphin-induced responses was identified
to be on nociceptor endings, because the responses were markedly
attenuated by intrathecal pretreatments with G
i1 or
Gi2 antisense-oligodeoxynucleotides. Similar mechanisms were observed with histamine-induced nociceptive responses, except for
the use of different antagonist and Gq/11
antisense-oligodeoxynucleotide. Both responses were characterized to be
mediated through inositol trisphosphate receptor-gated Ca2+
influx, because they were blocked by xestospongin C, an allosteric antagonist for inositol trisphosphate receptor and EGTA, but not thapsigargin. Because the nociceptive responses by compound 48/80 through histamine-release from mast cells were completely abolished by
thapsigargin, it is unlikely that the dose of thapsigargin is not
sufficient to block both responses. All of these in vivo findings
strongly support our previous view that kyotorphin elicits Ca2+ influx through inositol trisphosphate receptor located
at presynaptic plasma membranes.
This article has been cited by other articles:
|
|
 |
|
  M. Machuqueiro and A. M. Baptista The pH-Dependent Conformational States of Kyotorphin: A Constant-pH Molecular Dynamics Study Biophys. J., March 15, 2007; 92(6): 1836 - 1845. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. Mizota and H. Ueda Endocrine Disrupting Chemical Atrazine Causes Degranulation through Gq/11 Protein-Coupled Neurosteroid Receptor in Mast Cells Toxicol. Sci., April 1, 2006; 90(2): 362 - 368. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Inoue, T. Kawashima, R. G. Allen, and H. Ueda Nocistatin and Prepro-Nociceptin/Orphanin FQ 160-187 Cause Nociception through Activation of Gi/o in Capsaicin-Sensitive and of Gs in Capsaicin-Insensitive Nociceptors, Respectively J. Pharmacol. Exp. Ther., July 1, 2003; 306(1): 141 - 146. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. H. Rashid, M. Inoue, S. Kondo, T. Kawashima, S. Bakoshi, and H. Ueda Novel Expression of Vanilloid Receptor 1 on Capsaicin-Insensitive Fibers Accounts for the Analgesic Effect of Capsaicin Cream in Neuropathic Pain J. Pharmacol. Exp. Ther., March 1, 2003; 304(3): 940 - 948. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Inoue, S. Matsunaga, M. H. Rashid, A. Yoshida, K. Mizuno, T. Sakurada, H. Takeshima, and H. Ueda Pronociceptive Effects of Nociceptin/Orphanin FQ (13-17) at Peripheral and Spinal Level in Mice J. Pharmacol. Exp. Ther., October 1, 2001; 299(1): 213 - 219. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H. Ueda, M. Inoue, A. Yoshida, K. Mizuno, H. Yamamoto, J. Maruo, K. Matsuno, and S. Mita Metabotropic Neurosteroid/sigma -Receptor Involved in Stimulation of Nociceptor Endings of Mice J. Pharmacol. Exp. Ther., August 1, 2001; 298(2): 703 - 710. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. Tanimura, Y. Tojyo, and R. J. Turner Evidence That Type I, II, and III Inositol 1,4,5-Trisphosphate Receptors Can Occur as Integral Plasma Membrane Proteins J. Biol. Chem., August 25, 2000; 275(35): 27488 - 27493. [Abstract] [Full Text] [PDF]
|
|
 |
 |
 |
|
 |
 |
 |
