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001-es BibID:BIBFORM050448
Első szerző:Sántha Péter
Cím:The endogenous cannabinoid anandamide inhibits transient receptor potential vanilloid type 1 receptor-mediated currents in rat cultured primary sensory neurons / P. Sántha, Á. Jenes, Cs. Somogyi, I. Nagy
Dátum:2010
ISSN:0231-424X 1588-2683
Megjegyzések:The activity of the transient receptor potential vanilloid type 1 ion channel (TRPV1) that is expressed by the great majority of polymodal nociceptors is pivotal for the development of inflammatory heat hyperalgesia. The responsiveness of TRPV1 is regulated by a series of intracellular signalling molecules including the cyclic adenosine monophosphate (cAMP)-dependent protein kinase A (PKA); increased or decreased PKA activity results in TRPV1 sensitisation or desensitisation, respectively. Activation of the cannabinoid 1 (CB1) receptor that is expressed by the majority of the TRPV1-expressing primary sensory neurons reduces PKA activity. Therefore, here we studied whether activation of the CB1 receptor resulted in reduced TRPV1-mediated responses in cultured rat primary sensory neurons. We found that TRPV1-mediated whole-cell currents were significantly reduced respectively, by 50% and 25% by 10 nM and 30 nM of the endogenous CB1 receptor agonist, anandamide. The PKA inhibitor, H89 also had a significant inhibitory effect on TRPV1-mediated currents (~70%). These findings suggest that activation of the CB1 receptor can reduce the activity of TRPV1 in primary sensory neurons, and that this inhibitory effect could be mediated through the reduction of PKA-mediated phosphorylation of TRPV1.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény hazai lapban
anandamide
capsaicin
heat hyperalgesia
inflammation
TRPV1
nociception
vanilloid
PKA
Megjelenés:Acta Physiologica Hungarica. - 97 : 2 (2010), p. 149-158. -
További szerzők:Jenes Ágnes (1980-) (élettanász) Somogyi Csilla (1983-) (biológus, angol-magyar szakfordító) Nagy Istvan
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2.

001-es BibID:BIBFORM069011
Első szerző:Sousa-Valente, Joao
Cím:Inflammation of peripheral tissues and injury to peripheral nerves induce differing effects in the expression of the calcium-sensitive N-arachydonoylethanolamine-synthesizing enzyme and related molecules in rat primary sensory neurons / Sousa-Valente Joao, Varga Angelika, Torres-Perez Jose Vicente, Jenes Agnes, Wahba John, Mackie Ken, Cravatt Benjamin, Ueda Natsuo, Tsuboi Kazuhito, Santha Peter, Jancso Gabor, Tailor Hiren, Avelino António, Nagy Istvan
Dátum:2017
ISSN:0021-9967
Megjegyzések:Elevation of intracellular Ca2+ concentration induces the synthesis of N-arachydonoylethanolamine (anandamide) in a subpopulation of primary sensory neurons. N-acylphosphatidylethanolamine phospholipase D (NAPE-PLD) is the only known enzyme that synthesizes anandamide in a Ca2+ -dependent manner. NAPE-PLD mRNA as well as anandamide's main targets, the excitatory transient receptor potential vanilloid type 1 ion channel (TRPV1), the inhibitory cannabinoid type 1 (CB1) receptor, and the main anandamide-hydrolyzing enzyme fatty acid amide hydrolase (FAAH), are all expressed by subpopulations of nociceptive primary sensory neurons. Thus, NAPE-PLD, TRPV1, the CB1 receptor, and FAAH could form an autocrine signaling system that could shape the activity of a major subpopulation of nociceptive primary sensory neurons, contributing to the development of pain. Although the expression patterns of TRPV1, the CB1 receptor, and FAAH have been comprehensively elucidated, little is known about NAPE-PLD expression in primary sensory neurons under physiological and pathological conditions. This study shows that NAPE-PLD is expressed by about one-third of primary sensory neurons, the overwhelming majority of which also express nociceptive markers as well as the CB1 receptor, TRPV1, and FAAH. Inflammation of peripheral tissues and injury to peripheral nerves induce differing but concerted changes in the expression pattern of NAPE-PLD, the CB1 receptor, TRPV1, and FAAH. Together these data indicate the existence of the anatomical basis for an autocrine signaling system in a major proportion of nociceptive primary sensory neurons and that alterations in that autocrine signaling by peripheral pathologies could contribute to the development of both inflammatory and neuropathic pain.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
cannabinoid type 1 receptor
fatty acid amide hydrolase
inflammation
neuropathy
pain
transient receptor potential vanilloid type 1 ion channel
Megjelenés:Journal Of Comparative Neurology 525 : 8 (2017), p. 1778-1796. -
További szerzők:Varga Angelika (1977-) (biológus) Torres-Pérez, Jose Vicente Jenes Ágnes (1980-) (élettanász) Wahba, John Mackie, Ken Cravatt, Benjamin Ueda, Natsuo Tsuboi, Kazuhito Sántha Péter Jancsó Gábor Tailor, Hiren Avelino, Antonio Nagy István (orvos)
Pályázati támogatás:TAMOP 4.1.2. E-13/1/KONV-2013-0010
TÁMOP
K-101873
OTKA
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3.

001-es BibID:BIBFORM050443
035-os BibID:PMID:21056583
Első szerző:White, John P. M.
Cím:Xenon reduces activation of transient receptor potential vanilloid type 1 (TRPV1) in rat dorsal root ganglion cells and in human TRPV1-expressing HEK293 cells / John P. M. White, Guy Calcott, Agnes Jenes, Mahmuda Hossein, Cleoper C. Paule, Peter Santha, John B. Davis, Daqing Ma, Andrew S. C. Rice, Istvan Nagy
Dátum:2011
ISSN:0024-3205
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Life Sciences. - 88 : 3-4 (2011), p. 141-149. -
További szerzők:Calcott, Guy Jenes Ágnes (1980-) (élettanász) Hossein, Mahmuda Paule, Cleoper C. Sántha Péter Davis, John B. Ma, Daqing Rice, Andrew S. C. Nagy István
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