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2008 ◽  
Vol 105 (2) ◽  
pp. 414-423 ◽  
Author(s):  
Seyeon Park ◽  
Eun Sook Ahn ◽  
Dong Woo Han ◽  
Jong Hwa Lee ◽  
Kyung Tae Min ◽  
...  


Pain ◽  
2000 ◽  
Vol 84 (1) ◽  
pp. 13-20 ◽  
Author(s):  
Carolyn A. Fairbanks ◽  
Ivan J. Posthumus ◽  
Kelley F. Kitto ◽  
Laura S. Stone ◽  
George L. Wilcox


1999 ◽  
Vol 276 (4) ◽  
pp. C915-C922 ◽  
Author(s):  
J. T. Seo ◽  
H. Sugiya ◽  
S. I. Lee ◽  
M. C. Steward ◽  
A. C. Elliott

We used the Ca2+-sensitive fluorescent dye fura 2, together with measurements of intracellulard- myo-inositol 1,4,5-trisphosphate [Ins(1,4,5) P 3], to assess the inhibitory effects of caffeine on signal transduction via G protein-coupled receptor pathways in isolated rat mandibular salivary acinar cells. ACh, norepinephrine (NE), and substance P (SP) all evoked substantial increases in the intracellular free Ca2+ concentration ([Ca2+]i). Responses to ACh and NE were markedly inhibited by prior application of 20 mM caffeine. The inhibitory effect of caffeine was not reproduced by phosphodiesterase inhibition with IBMX or addition of cell-permeant dibutyryl cAMP. In contrast to the ACh and NE responses, the [Ca2+]iresponse to SP was unaffected by caffeine. Despite this, SP and ACh appeared to mobilize Ca2+ from a common intracellular pool. Measurements of agonist-induced changes in Ins(1,4,5) P 3levels confirmed that caffeine inhibited the stimulus-response coupling pathway at a point before Ins(1,4,5) P 3generation. Caffeine did not, however, inhibit [Ca2+]iresponses evoked by direct activation of G proteins with 40 mM F−. These data show that caffeine inhibits G protein-coupled signal transduction in these cells at some element that is common to the muscarinic and α-adrenergic signaling pathways but is not shared by the SP signaling pathway. We suggest that this element might be a specific structural motif on the G protein-coupled muscarinic and α-adrenergic receptors.



Life Sciences ◽  
1998 ◽  
Vol 62 (21) ◽  
pp. PL319-PL325 ◽  
Author(s):  
So-Rah Yoon ◽  
Jin-Ju Nah ◽  
Young-Hee Shin ◽  
Si-Kwan Kim ◽  
Ki-Youl Nam ◽  
...  


1995 ◽  
Vol 39 (6) ◽  
pp. 383
Author(s):  
Y-M. LI ◽  
D. E. WINGROVE ◽  
H. P. TOO ◽  
M. MARNERAKIS ◽  
E. R. STIMSON ◽  
...  


1995 ◽  
Vol 73 (7) ◽  
pp. 871-877 ◽  
Author(s):  
D. T. Beattie ◽  
H. E. Connor ◽  
R. M. Hagan

The role of substance P and the influence of neurokinin 1 (NK1) receptor antagonists in the cranial circulation are described in the present review, particularly with respect to the mechanisms involved in the etiology of migraine headache. Substance P is distributed throughout the cranial vasculature, in the trigeminal sensory afferent nerve fibres, and its release can be demonstrated following activation of the trigeminovascular system in animals and humans. Following its release and NK1 receptor activation, dilatation and edema result, two events that are implicated in the pathogenesis of migraine headache. The recently developed selective NK1 receptor antagonists inhibit substance P mediated dilatation and plasma protein extravasation in the cranial circulation, suggesting that they may provide an effective and novel acute treatment for migraine.Key words: substance P, migraine, NK1 receptor antagonists.



1995 ◽  
Vol 82 (1) ◽  
pp. 166-173 ◽  
Author(s):  
Yue-Ming Li ◽  
Douglas E. Wingrove ◽  
Phon H. Too ◽  
Margarita Marnerakis ◽  
Evelyn R. Stimson ◽  
...  

Background During spinal and epidural anesthesia, local anesthetics reach concentrations in cerebrospinal fluid and spinal cord tissues at which their actions may extend beyond the classic blockade of sodium channels. This study examines the effects of several clinical and experimental local anesthetics on the binding and actions of a peptide neurotransmitter, substance P, known to be important in nociceptive transmission in the dorsal horn. Methods The binding of radiolabeled (Bolton-Hunter modified) substance P was studied in chick brain membranes in the presence of local anesthetics. The increase in intracellular calcium [Ca2+]in evoked by substance P was measured by the fluorescent indicator fura-2 loaded in a murine cell line expressing substance P (NK1) receptors. Cells were preincubated with bupivacaine before and during the transient addition of substance P. Results Both substance P binding and Ca2+ increase were inhibited half-maximally by approximately 1 mM bupivacaine at pH 7.5, whereas tetracaine, lidocaine, and benzocaine were slightly less potent at inhibiting binding. Concentration-dependent substance P-binding studies showed that bupivacaine's inhibition was not competitive. Inhibition of substance P binding by bupivacaine increased with increasing pH, but the protonated species appears to have some inhibitory activity, and quaternary lidocaine also inhibited binding. There was no stereoselectively to the binding inhibition. Conclusions Because millimolar concentrations of local anesthetics are within the range measured in spinal cord during intrathecal and epidural procedures, these results are consistent with a direct action of local anesthetics on tachykinin-mediated neurotransmission during regional anesthesia.



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