Pregabalin and gabapentin inhibit substance P-induced NF-κB activation in neuroblastoma and glioma cells

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

Caffeine does not inhibit substance P-evoked intracellular Ca2+ mobilization in rat salivary acinar cells

1999 ◽  
Vol 276 (4) ◽  
pp. C915-C922 ◽  
Author(s):  
J. T. Seo ◽  
H. Sugiya ◽  
S. I. Lee ◽  
M. C. Steward ◽  
A. C. Elliott
Keyword(s):  
Signal Transduction ◽  
Substance P ◽  
G Protein ◽  
Acinar Cells ◽  
Inhibitory Effect ◽  
Structural Motif ◽  
Stimulus Response ◽  
Inhibit Substance ◽  
Prior Application ◽  
G Protein Coupled

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.

scholarly journals Sufentanil, Morphine, Met-enkephalin, and k-Agonist (U-50,488H) Inhibit Substance P Release from Primary Sensory Neurons

1989 ◽  
Vol 70 (4) ◽  
pp. 672-677 ◽  
Author(s):  
H. Ming Chang ◽  
Charles B. Berde ◽  
George G. Holz ◽  
Grieg F. Steward ◽  
Richard M. Kream
Keyword(s):  
Substance P ◽  
Sensory Neurons ◽  
Primary Sensory Neurons ◽  
P Release ◽  
Inhibit Substance ◽  
Substance P Release

Adenosine and 5-HT inhibit substance P release from nerve endings in myenteric ganglia by distinct mechanisms

1993 ◽  
Vol 264 (3) ◽  
pp. G454-G461 ◽  
Author(s):  
R. M. Broad ◽  
T. J. McDonald ◽  
M. A. Cook
Keyword(s):  
Substance P ◽  
Nerve Endings ◽  
Enteric Ganglia ◽  
Adenosine A1 ◽  
Inhibit Substance ◽  
A1 Receptor ◽  
K Concentration ◽  
Prejunctional Inhibition ◽  
Substance P Release ◽  
Myenteric Ganglia

Release of substance P-like immunoreactivity (SP-LI) from dissociated enteric ganglia and the receptor-mediated prejunctional inhibition of this release were investigated with the use of a perifusion technique. SP-LI release was evoked by elevated extracellular K+ concentration and was inhibited, in a graded manner, by N6-cyclopentyl adenosine (CPA), an adenosine analogue with selectivity for adenosine A1 receptors. Similar inhibition of SP-LI release was obtained with 5-hydroxytryptamine (5-HT); incrementing concentrations, however, yielded a biphasic concentration-response relationship. The selective adenosine A1 receptor antagonist 1,3-dipropyl-8-cyclopentyl-xanthine abolished the inhibition due to CPA, whereas the inhibitory action of 5-HT was sensitive to the 5-HT1A-selective antagonist 1-(2-methoxyphenyl)-4-[4-(2-phthalimido)butyl]-piperazine hydrobromide. Inhibition due to both agonists was insensitive to blockade by tetrodotoxin, suggesting a prejunctional locus for both adenosine and 5-HT1A receptors on the tachykininergic nerve endings. Pretreatment of ganglia with pertussis toxin had no effect on CPA-mediated inhibition of SP-LI release, whereas 5-HT-mediated inhibition was abolished. The findings demonstrate that adenosine and 5-HT receptors on enteric nerve endings are coupled to inhibition of tachykinin release through distinct mechanisms, putatively distinct G proteins.

scholarly journals Pyrrolomycin group antibiotics inhibit substance P-induced release of myeloperoxidase from human polymorphonuclear leukocytes.

1991 ◽  
Vol 44 (5) ◽  
pp. 533-540 ◽  
Author(s):  
KAORI MASUDA ◽  
KAZUO SUZUKI ◽  
AKIKO ISHIDA-OKAWARA ◽  
SATOSHI MIZUNO ◽  
KUNIMOTO HOTTA ◽  
...  
Keyword(s):  
Substance P ◽  
Polymorphonuclear Leukocytes ◽  
Inhibit Substance ◽  
Human Polymorphonuclear Leukocytes

Involvement of endopeptidase-24.11 in degradation of substance P by glioma cells

Neuropeptides ◽  
1989 ◽  
Vol 14 (3) ◽  
pp. 177-184 ◽  
Author(s):  
S. Endo ◽  
H. Yokosawa ◽  
S. Ishii
Keyword(s):  
Substance P ◽  
Glioma Cells ◽  
Endopeptidase 24.11

Recent developments in tachykinin NK1 receptor antagonists: prospects for the treatment of migraine headache

1995 ◽  
Vol 73 (7) ◽  
pp. 871-877 ◽  
Author(s):  
D. T. Beattie ◽  
H. E. Connor ◽  
R. M. Hagan
Keyword(s):  
Substance P ◽  
Migraine Headache ◽  
Receptor Activation ◽  
Receptor Antagonists ◽  
Trigeminovascular System ◽  
Protein Extravasation ◽  
Recent Developments ◽  
Inhibit Substance ◽  
Neurokinin 1 ◽  
Nk1 Receptor Antagonists

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.

Local Anesthetics Inhibit Substance P Binding and Evoked Increases in Intracellular Calcium sup 2+ 

1995 ◽  
Vol 82 (1) ◽  
pp. 166-173 ◽  
Author(s):  
Yue-Ming Li ◽  
Douglas E. Wingrove ◽  
Phon H. Too ◽  
Margarita Marnerakis ◽  
Evelyn R. Stimson ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Substance P ◽  
Intracellular Calcium ◽  
Local Anesthetics ◽  
Competitive Inhibition ◽  
Direct Action ◽  
Binding Studies ◽  
Nociceptive Transmission ◽  
Murine Cell Line ◽  
Inhibit Substance

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.

Opiate analgesics inhibit substance P release from rat trigeminal nucleus

Pain ◽  
1979 ◽  
Vol 6 (3) ◽  
pp. 385-386
Author(s):  
T. M. Jessell ◽  
L. L. Iversen
Keyword(s):  
Substance P ◽  
Trigeminal Nucleus ◽  
P Release ◽  
Inhibit Substance ◽  
Opiate Analgesics ◽  
Substance P Release

Eosinophil granule proteins inhibit substance P-induced histamine release from human skin mast cells

1994 ◽  
Vol 93 (5) ◽  
pp. 900-909 ◽  
Author(s):  
Y OKAYAMA ◽  
S EILATI ◽  
K LEIFERMAN ◽  
M CHURCH
Keyword(s):  
Mast Cells ◽  
Substance P ◽  
Histamine Release ◽  
Human Skin ◽  
Eosinophil Granule Proteins ◽  
Inhibit Substance ◽  
Granule Proteins ◽  
Eosinophil Granule
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