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1.

001-es BibID:BIBFORM001452
Első szerző:Baiou, Djalil
Cím:Neurochemical characterisation of insulin receptor-expressing primary sensory neurons in wild type and vanilloid type 1 transient receptor potential receptor knock-out mice / Baiou D., Santha P., Avelino A., Charrua A., Bácskai T., Matesz K., Cruz F., Nagy I.
Dátum:2007
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:The Journal of comparative neurology 503 : 2 (2007), p. 334-347. -
További szerzők:Sántha Péter Avelino, Antonio Charrua, Ana Bácskai Tímea (1974-) (biológus, neurobiológus) Matesz Klára (1949-) (anatómus, neurobiológus) Cruz, Francisco Nagy István (orvos)
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2.

001-es BibID:BIBFORM029521
Első szerző:Sathianathan, Vivian
Cím:Insulin induces cobalt uptake in a subpopulation of rat cultured primary sensory neurons / Sathianathan Vivian, Avelino Antonio, Charrua Ana, Santha Peter, Matesz Klara, Cruz Francisco, Nagy Istvan
Dátum:2003
ISSN:0953-816X
Megjegyzések:Previous findings show that both the vanilloid receptor 1 and the insulin receptor are expressed on small primary sensory neurons. As insulin evokes activity in second messengers which could induce opening of the vanilloid receptor 1, we examined, by using the cobalt-uptake technique, whether or not insulin can activate cultured rat primary sensory neurons through activating the vanilloid receptor 1. Capsaicin (50, 100 and 500 nm) induced concentration-dependent labelling in primary sensory neurons. Preincubation of cells in insulin (10 micromoles) for 10 min followed by a 2-min wash did not produce significant change in the capsaicin-induced labelling. Coapplication of insulin (10 micromoles) with capsaicin, however, potentiated the 50 and 100 nm capsaicin-evoked staining. Insulin itself also produced cobalt labelling in a concentration-dependent manner. The size-frequency distributions of neurons showing capsaicin- or insulin-induced cobalt accumulation were similar. The insulin-induced cobalt labelling was significantly reduced by the tyrosine kinase inhibitor, tyrphostin AG1024, the vanilloid receptor 1 antagonists, ruthenium red and capsazepine, the protein kinase inhibitor, staurosporine and the phospholipase C inhibitor neomycin. Double immunostaining of cultured primary sensory neurons and sections from dorsal root ganglia revealed that about one-third of the cells coexpress the insulin receptor and vanilloid receptor 1. These findings suggest that insulin activates a subpopulation of primary sensory neurons, probably through phosphorylation- and/or phosphatidylinositol(4,5)biphosphate hydrolysis-evoked activation of the vanilloid receptor 1. Although the insulin-induced activation of vanilloid receptor 1 seems to be a short-lived effect in vitro, in vivo it might play a role in the development of burning pain sensation in hyperinsulinism.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:European Journal Of Neuroscience 18 : 9 (2003), p. 2477-2486. -
További szerzők:Avelino, Antonio Charrua, Ana Sántha Péter Matesz Klára (1949-) (anatómus, neurobiológus) Cruz, Francisco Nagy István (orvos)
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3.

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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4.

001-es BibID:BIBFORM040293
Első szerző:Veress Gábor (neurobiológus)
Cím:Characterisation of cannabinoid 1 receptor expression in the perikarya, and peripheral and spinal processes of primary sensory neurons / Veress Gabor, Meszar Zoltan, Muszil Dora, Avelino Antonio, Matesz Klara, Mackie Ken, Nagy Istvan
Dátum:2013
ISSN:1863-2653
Megjegyzések:The cannabinoid 1 (CB1) receptor is expressed by a sub-population of primary sensory neurons. However, data on the neurochemical identity of the CB1 receptor-expressing cells, and CB1 receptor expression by the peripheral and central terminals of these neurons are inconsistent and limited. We characterised CB1 receptor expression in dorsal root ganglia (DRG) and spinal cord at the lumbar 4-5 level, as well as in the urinary bladder and glabrous skin of the hindpaw. About 1/3 of DRG neurons exhibited immunopositivity for the CB1 receptor, the majority of which showed positivity for the nociceptive markers calcitonin gene-related peptide (CGRP) or/and Griffonia (bandeiraea) simplicifolia IB4 isolectin-binding. Virtually all CB1 receptor-immunostained fibres showed immunopositivity for CGRP in the skin, while very few did in the urinary bladder. No CB1 receptor-immunopositive nerve fibres were IB4 positive in either peripheral tissue. Spinal laminae I and II-outer showed the highest density of CB1 receptor-immunopositive punctae, the majority of which showed positivity for CGRP or/and IB4 binding. These data indicate that a major sub-population of nociceptive primary sensory neurons expresses CB1 receptors that are transported to both peripheral and central terminals of these cells. Therefore, the present data suggest that manipulation of endogenous CB1 receptor agonist levels in these areas may significantly reduce nociceptive input into the spinal cord.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Brain Structure & Function. - 218 : 3 (2013), p. 733-750. -
További szerzők:Mészár Zoltán Mihály (1977-) (agrármérnök) Muszil Dóra Avelino, Antonio Matesz Klára (1949-) (anatómus, neurobiológus) Mackie, Ken Nagy István (orvos)
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5.

001-es BibID:BIBFORM020455
Első szerző:White, John P. M.
Cím:Severe burn injury induces a characteristic activation of extracellular signal-regulated kinase 1/2 in spinal dorsal horn neurons / John P. M. White, Chin Wing Ko, Antonio Rei Fidalgo, Mario Cibelli, Cleoper C. Paule, Peter J. Anderson, Celia Cruz, Szabolcs Gomba, Klara Matesz, Gabor Veress, Antonio Avelino, Istvan Nagy
Dátum:2011
ISSN:1090-3801
Megjegyzések:We have studied scalding-type burn injury-induced activation of extracellular signal-regulated kinase 1/2 (ERK1/2) in the spinal dorsal horn, which is a recognised marker for spinal nociceptive processing. At 5min after severe scalding injury to mouse hind-paw, a substantial number of phosphorylated ERK1/2 (pERK1/2) immunopositive neurons were found in the ipsilateral dorsal horn. At 1h post-injury, the number of pERK1/2-labelled neurons remained substantially the same. However, at 3h post-injury, a further increase in the number of labelled neurons was found on the ipsilateral side, while a remarkable increase in the number of labelled neurons on the contralateral side resulted in there being no significant difference between the extent of the labelling on both sides. By 6h post-injury, the number of labelled neurons was reduced on both sides without there being significant difference between the two sides. A similar pattern of severe scalding injury-induced activation of ERK1/2 in spinal dorsal horn neurons over the same time-course was found in mice which lacked the transient receptor potential type 1 receptor (TRPV1) except that the extent to which ERK1/2 was activated in the ipsilateral dorsal horn at 5 min post-injury was significantly greater in wild-type animals when compared to TRPV1 null animals. This difference in activation of ERK1/2 in spinal dorsal horn neurons was abolished within 1h after injury, demonstrating that TRPV1 is not essential for the maintenance of ongoing spinal nociceptive processing in inflammatory pain conditions in mouse resulting from at least certain types of severe burn injury.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:European Journal of Pain. - 15 : 7 (2011), p. 683-690. -
További szerzők:Ko, Chin Wing Fidalgo, Antonio Rei Cibelli, Mario Paule, Cleoper C. Anderson, Peter J. Cruz, Celia Gomba Szabolcs (1933-2016) (pathológus) Matesz Klára (1949-) (anatómus, neurobiológus) Veress Gábor (1971-) (neurobiológus) Avelino, Antonio Nagy István (orvos)
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