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001-es BibID:	BIBFORM050560
Első szerző:	Mistry, Shilpa
Cím:	Prolonged exposure to bradykinin and prostaglandin E2 increases TRPV1 mRNA but does not alter TRPV1 and TRPV1b protein expression in cultured rat primary sensory neurons / Shilpa Mistry, Cleoper C. Paule, Angelika Varga, Andy Photiou, Agnes Jenes, Antonio Avelino, Laki Buluwela, Istvan Nagy
Dátum:	2014
ISSN:	0304-3940
Megjegyzések:	Sensitisation of the capsaicin receptor, transient receptor potential vanilloid type 1 (TRPV1) ion channel in nociceptive primary sensory neurons (PSN) underlies the development of inflammatory heat hyperalgesia. Removal of the negative-dominant splice variant of the TRPV1 molecule, TRPV1b from TRPV1/TRPV1b heterotetrameric channels, which should be associated with changes in the expression of TRPV1 and TRPV1b transcripts and proteins, has been suggested to contribute to that sensitisation. Respective reverse-transcriptase polymerase chain reaction (RT-PCR) and Western-blotting revealed that both TRPV1 and TRPV1b mRNA, and their encoded proteins are expressed in rat cultured PSN. Sequencing of the RT-PCR products showed that TRPV1b mRNA lacks the entire exon 7. Further, growing PSN for 2 days in the presence of 10műM bradykinin (BK) and 10műM prostaglandin E2 (PGE2) significantly increases TRPV1 responsiveness and TRPV1 mRNA expression, without producing any changes in TRPV1b mRNA, and TRPV1 and TRPV1b protein expression. These data challenge the hypothesis that alterations in the composition of the TRPV1 ion channel contributes to the sensitisation.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:	Neuroscience Letters. - 564 (2014), p. 89-93. -
További szerzők:	Paule, Cleoper C. Varga Angelika (1977-) (biológus) Photiou, Andy Jenes Ágnes (1980-) (élettanász) Avelino, Antonio Buluwela, Laki Nagy István
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM060177
Első szerző:	Sousa-Valente, Joao
Cím:	Anandamide in primary sensory neurons: too much of a good thing? / Joao Sousa-Valente, Angelika Varga, Kajaluxy Ananthan, Ankur Khajuria, Istvan Nagy
Dátum:	2014
ISSN:	0953-816X
Megjegyzések:	The quest for possible targets for the development of novel analgesics has identified the activation of the cannabinoid type 1 (CB1) receptor outside the CNS as a potential means of providing relief from persistent pain, which currently constitutes an unmet medical need. Increasing tissue levels of the CB1 receptor endogenous ligand N-arachidonoylethanolamine (anandamide), by inhibiting anandamide degradation through blocking the anandamide-hydrolysing enzyme fatty acid amide hydrolase, has been suggested to be used to activate the CB1 receptor. However, recent clinical trials revealed that this approach does not deliver the expected relief from pain. Here, we discuss one of the possible reasons, the activation of the transient receptor potential vanilloid type 1 ion channel (TRPV1) on nociceptive primary sensory neurons (PSNs) by anandamide, which may compromise the benefi- cial effects of increased tissue levels of anandamide. We conclude that better design such as concomitant blocking of anandamide hydrolysis and anandamide uptake into PSNs, to inhibit TRPV1 activation, could overcome these problems.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban analgesics cannabinoid dorsal root ganglia endogenous cannabinoids TRPV1
Megjelenés:	European Journal Of Neuroscience. - 39 : 3 (2014), p. 409-418. -
További szerzők:	Varga Angelika (1977-) (biológus) Ananthan, Kajaluxy Khajuria, Ankur Nagy István
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM071121
035-os BibID:	(WoS)000419131300008 (Scopus)85031925522
Első szerző:	Torres-Pérez, Jose Vicente
Cím:	The NAv1.7 blocker protoxin II reduces burn injury-induced spinal nociceptive processing / Jose Vicente Torres-Pérez, Pavel Adamek, Jiri Palecek, Marcela Vizcaychipi, Istvan Nagy, Angelika Varga
Dátum:	2018
ISSN:	0946-2716
Megjegyzések:	Controlling pain in burn-injured patients poses a major clinical challenge. Recent findings suggest that reducing the activity of the voltage-gated sodium channel Nav1.7 in primary sensory neurons could provide improved pain control in burn-injured patients. Here, we report that partial thickness scalding-type burn injury on the rat paw upregulates Nav1.7 expression in primary sensory neurons 3 h following injury. The injury also induces upregulation in phosphorylated cyclic adenosine monophosphate response element-binding protein (p-CREB), a marker for nociceptive activation in primary sensory neurons. The upregulation in p-CREB occurs mainly in Nav1.7-immunopositive neurons and exhibits a peak at 5 min and, following a decline at 30 min, a gradual increase from 1 h post-injury. The Nav1.7 blocker protoxin II (ProTxII) or morphine injected intraperitoneally 15 min before or after the injury significantly reduces burn injury-induced spinal upregulation in phosphorylated serine 10 in histone H3 and phosphorylated extracellular signal-regulated kinase 1/2, which are both markers for spinal nociceptive processing. Further, ProTxII significantly reduces the frequency of spontaneous excitatory post-synaptic currents in spinal dorsal horn neurons following burn injury. Together, these findings indicate that using Nav1.7 blockers should be considered to control pain in burn injury.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk Pain Primary sensory neuron Spinal cord p-ERK1/2 p-S10H3
Megjelenés:	Journal of Molecular Medicine. Berlin, Germany. - 96 : 1 (2018), p. 75-84. -
További szerzők:	Adamek, Pavel Palecek, Jiri Vizcaychipi, Marcela Nagy István Varga Angelika (1977-) (biológus)
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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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