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001-es BibID:	BIBFORM050561
035-os BibID:	PMID:24114173
Első szerző:	Varga Angelika (biológus)
Cím:	Anandamide produced by Ca2+-insensitive enzymes induces excitation in primary sensory neurons / Angelika Varga, Agnes Jenes, Timothy H. Marczylo, Joao Sousa-Valente, Jie Chen, Jonothan Austin, Srikumaran Selvarajah, Fabiana Piscitelli, Anna P. Andreou, Anthony H. Taylor, Fiona Kyle, Mohammed Yaqoob, Sue Brain, John P. M. White, Laszlo Csernoch, Vincenzo Di Marzo, Laki Buluwela, Istvan Nagy
Dátum:	2014
ISSN:	0031-6768
Megjegyzések:	The endogenous lipid agent N-arachidonoylethanolamine (anandamide), among other effects, has been shown to be involved in nociceptive processing both in the central and peripheral nervous systems. Anandamide is thought to be synthesised by several enzymatic pathways both in a Ca2+-sensitive and Ca2+-insensitive manner, and rat primary sensory neurons produce anandamide. Here, we show for the first time, that cultured rat primary sensory neurons express at least four of the five known Ca2+-insensitive enzymes implicated in the synthesis of anandamide, and that application of 1,2-dioleoyl-sn-glycero-3-phosphoethanolamine-N-arachidonoyl, the common substrate of the anandamide-synthesising pathways, results in anandamide production which is not changed by the removal of extracellular Ca2+. We also show that anandamide, which has been synthesised in primary sensory neurons following the application of 1,2-dioleoyl-sn-glycero-3-phosphoethanolamine-N-arachidonoyl induces a transient receptor potential vanilloid type 1 ion channel-mediated excitatory effect that is not inhibited by concomitant activation of the cannabinoid type 1 receptor. Finally, we show that sub-populations of transient receptor potential vanilloid type 1 ion channel-expressing primary sensory neurons also express some of the putative Ca2+-insensitive anandamide-synthesising enzymes. Together, these findings indicate that anandamide synthesised by primary sensory neuron via a Ca2+-insensitive manner has an excitatory rather than an inhibitory role in primary sensory neurons and that excitation is mediated predominantly through autocrine signalling. Regulation of the activity of the Ca2+-insensitive anandamide-synthesising enzymes in these neurons may be capable of regulating the activity of these cells, with potential relevance to controlling nociceptive processing.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:	Pflugers Archiv. - 466 : 7 (2014), p. 1421-1435. -
További szerzők:	Jenes Ágnes (1980-) (élettanász) Marczylo, Timothy H. Sousa-Valente, Joao Chen, Jie Austin, Jonothan Selvarajah, Srikumaran Piscitelli, Fabiana Andreou, Anna P. Taylor, Anthony H. Kyle, Fiona Yaqoob, Mohammed Brain, Sue White, John P. M. Csernoch László (1961-) (élettanász) Di Marzo, Vincenzo Buluwela, Laki Nagy István
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM050442
035-os BibID:	PMID:20038442
Első szerző:	White, John P. M.
Cím:	Sensitization of the transient receptor potential vanilloid type 1 ion channel by isoflurane or sevoflurane does not result in extracellular signal-regulated kinase 1/2 activation in rat spinal dorsal horn neurons / J. P. M. White, M. Cibelli, A. R. Fidalgo, C. C. Paule, P. J. Anderson, A. Jenes, A. S. C. Rice, I. Nagy
Dátum:	2010
ISSN:	0306-4522
Megjegyzések:	Clinically relevant concentrations of isoflurane or sevoflurane sensitize transient receptor potential vanilloid type 1 to several of its activators, including capsaicin. It has, moreover, been suggested these volatile general anaesthetics may augment nociceptive signalling arising from surgical procedures and thereby contribute to post-operative pain. To investigate this suggestion, we have studied intraplantar capsaicin injection-induced phosphorylation of extracellular signal-regulated kinase 1/2 in spinal dorsal horn neurons (which is a recognized marker of spinal nociceptive processing) in rat during isoflurane or sevoflurane anaesthesia after 60 min under anaesthesia. Control animals were anaesthetized with pentobarbital (which of itself does not activate extracellular signal-regulated kinase 1/2 in spinal dorsal horn neurons). Unilateral intraplantar capsaicin injection in control animals evoked extracellular signal-regulated kinase 1/2 phosphorylation in a group of neurons in lamina I and lamina II of the ipsilateral spinal dorsal horn in a somatotopically appropriate area. In contrast, both anaesthetic gases (given for 60 min and without subsequent capsaicin injection) induced extracellular signal-regulated kinase 1/2 activation in a different group of mainly lamina I neurons bilaterally. The total number of spinal dorsal horn neurons labelled on the ipliateral side following capsaicin injection into the isoflurane-, or sevoflurane-, anaesthetized animals was significantly less than that produced by capsaicin alone. Further, capsaicin injection into isoflurane-, or sevoflurane-, anaesthetized animals reduced extracellular signal-regulated kinase 1/2 phosphorylation induced by the gases alone on both sides. These findings do not support the suggestion that isoflurane-, or sevoflurane-, induced sensitization of transient receptor potential vanilloid type 1 by capsaicin, or other agonist, is translated into induction of spinal nociceptive processing and consequential pain sensation.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:	Neuroscience. - 166 : 2 (2010), p. 633-638. -
További szerzők:	Cibelli, Mario Fidalgo, Antonio Rei Paule, Cleoper C. Anderson, Peter J. Jenes Ágnes (1980-) (élettanász) Rice, Andrew S. C. Nagy István
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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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
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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