TY - JOUR AU - Al-omari, Ammar AU - Kecskés, Miklós AU - Gaszner, Balázs AU - Biró-Sütő, Tünde AU - Fazekas, Balázs AU - Berta, Gergely AU - Kuzma, Mónika AU - Pintér, Erika AU - Kormos, Viktória TI - Functionally active TRPA1 ion channel is downregulated in peptidergic neurons of the Edinger-Westphal nucleus upon acute alcohol exposure JF - FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY J2 - FRONT CELL DEV BIOL VL - 10 PY - 2023 PG - 13 SN - 2296-634X DO - 10.3389/fcell.2022.1046559 UR - https://m2.mtmt.hu/api/publication/33553138 ID - 33553138 N1 - * Megosztott szerzőség AB - Introduction: The centrally projecting Edinger-Westphal nucleus (EWcp) contributes to the control of alcohol consumption by its urocortin 1 (UCN1) and cocaine- and amphetamine-regulated transcript (CART) co-expressing peptidergic neurons. Our group recently showed that the urocortinergic centrally projecting EWcp is the primary seat of central nervous system transient receptor potential ankyrin 1 (TRPA1) cation channel mRNA expression. Here, we hypothesized that alcohol and its metabolites, that pass through the blood-brain barrier, may influence the function of urocortinergic cells in centrally projecting EWcp by activating TRPA1 ion channels. We aimed to examine the functional activity of TRPA1 in centrally projecting EWcp and its possible role in a mouse model of acute alcohol exposure. LA - English DB - MTMT ER - TY - JOUR AU - Konkoly, János AU - Kormos, Viktória AU - Gaszner, Balázs AU - Correia, Pedro AU - Berta, Gergely AU - Biró-Sütő, Tünde AU - Zelena, Dóra AU - Pintér, Erika TI - Transient receptor potential ankyrin 1 ion channel expressed by the Edinger-Westphal nucleus contributes to stress adaptation in murine model of posttraumatic stress disorder JF - FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY J2 - FRONT CELL DEV BIOL VL - 10 PY - 2022 PG - 12 SN - 2296-634X DO - 10.3389/fcell.2022.1059073 UR - https://m2.mtmt.hu/api/publication/33293967 ID - 33293967 N1 - * Megosztott szerzőség AB - The centrally projecting Edinger-Westphal nucleus (EWcp) is involved in stress adaptation. Transient receptor potential ankyrin 1 (TRPA1) mRNA was previously shown to be expressed abundantly in mouse and human EWcp urocortin 1 (UCN1) positive neurons and reacted to chronic stress. Since UCN1 neurons are deeply implicated in stress-related disorders, we hypothesized that TRPA1/UCN1 neurons are also affected in posttraumatic stress disorder (PTSD). We examined male Trpa1 wild type (WT) and gene-deficient (KO) mice in the single prolonged stress (SPS) model of PTSD. Two weeks later the behavioral changes were monitored by forced swim test (FST) and restraint. The Trpa1 and Ucn1 mRNA expression and the UCN1 peptide content were assessed by RNAscope in situ hybridization technique combined with immunofluorescence labeling in the EWcp. SPS-induced immobility was lower in Trpa1 KO compared to WT animals, both in the FST and restraint, corresponding to diminished depression-like behavior. The copy number of Trpa1 mRNA decreased significantly in EWcp of WT animals in response to SPS. Higher basal Ucn1 mRNA expression was observed in the EWcp of KO animals, that was not affected by SPS exposure. EWcp neurons of WT animals responded to SPS with substantially increased amount of UCN1 peptide content compared to control animals, whereas such changes were not observable in KO mice. The decreased Trpa1 mRNA expression in the SPS model of PTSD associated with increased neuronal UCN1 peptide content suggests that this cation channel might be involved in the regulation of stress adaptation and may contribute to the pathomechanism of PTSD. LA - English DB - MTMT ER - TY - JOUR AU - Horváth, Ádám AU - Payrits, Maja AU - Steib, Anita AU - Kántás, Boglárka AU - Biró-Sütő, Tünde AU - Erostyák, János AU - Makkai, Géza AU - Sághy, Éva AU - Helyes, Zsuzsanna AU - Szőke, Éva TI - Analgesic Effects of Lipid Raft Disruption by Sphingomyelinase and Myriocin via Transient Receptor Potential Vanilloid 1 and Transient Receptor Potential Ankyrin 1 Ion Channel Modulation JF - FRONTIERS IN PHARMACOLOGY J2 - FRONT PHARMACOL VL - 11 PY - 2021 PG - 11 SN - 1663-9812 DO - 10.3389/fphar.2020.593319 UR - https://m2.mtmt.hu/api/publication/31848850 ID - 31848850 N1 - Funding Agency and Grant Number: National Brain Research Program [2017-1.2.1-NKP -2017-00002]; Hungarian Government [GINOP-2.3.2-15-2016-00050, EFOP-3.6.2-16-2017-00006, EFOP-3.6.2-16-2017-00008]; Janos Bolyai Research Scholarship of the Hungarian Academy of Sciences; University of Pecs [17886-4/23018/FEKUTSTRAT]; New National Excellence Program of the Ministry of Human Capacities [UNKP-18-4]; Gedeon Richter's Talentum Foundation; New National Excellence Program of the Ministry for Innovation and Technology [UNKP-19-4] Funding text: This work was supported by the National Brain Research Program 2017-1.2.1-NKP -2017-00002 (NAP-2; Chronic Pain Research Group). We acknowledge the grant of the Hungarian Government (GINOP-2.3.2-15-2016-00050, EFOP-3.6.2-16-2017-00006 and EFOP-3.6.2-16-2017-00008). ESz and ESa were supported by the Janos Bolyai Research Scholarship of the Hungarian Academy of Sciences. The University of Pecs is acknowledged for a support by the 17886-4/23018/FEKUTSTRAT excellence grant. MP was supported by the New National Excellence Program of the Ministry of Human Capacities UNKP-18-4. ESz and ESa were supported by the New National Excellence Program of the Ministry of Human Capacities UNKP-18-4 and New National Excellence Program of the Ministry for Innovation and TechnologyUNKP-19-4 grant. AHwas supported by the Gedeon Richter's Talentum Foundation. LA - English DB - MTMT ER - TY - CHAP AU - Payrits, Maja AU - Ádám, Horváth AU - Biró-Sütő, Tünde AU - János, Erostyák AU - Géza, Makkai AU - Sághy, Éva AU - Pohóczky, Krisztina AU - Kecskés, Angéla AU - Kecskés, Miklós AU - Szolcsányi, János AU - Helyes, Zsuzsanna AU - Szőke, Éva ED - Rakonczay, Zoltán ED - Kiss, Lóránd TI - Resolvin D1 and D2 inhibit Transient Receptor Potential Vanilloid 1 and Ankyrin 1 Ion Channel activation on sensory neurons via lipid raft modification T2 - Proceedings of the EFOP-3.6.2-16-2017-00006 (LIVE LONGER) project PB - University of Szeged CY - Szeged SN - 9789633067642 PY - 2020 SP - 59 EP - 59 PG - 1 UR - https://m2.mtmt.hu/api/publication/31684068 ID - 31684068 LA - English DB - MTMT ER - TY - JOUR AU - Szőke, Éva AU - Horvath, Adam AU - Biró-Sütő, Tünde AU - Sághy, Éva AU - Payrits, Maja AU - Erostyák, János AU - Makkai, Géza AU - Szolcsányi, János AU - Helyes, Zsuzsanna TI - In vitro and in vivo evidence for the role of lipid rafts in Ca2+-gating of the Transient Receptor Potential channels in sensory neurons JF - FASEB JOURNAL J2 - FASEB J VL - 34 PY - 2020 IS - S1 PG - 2 SN - 0892-6638 DO - 10.1096/fasebj.2020.34.s1.05167 UR - https://m2.mtmt.hu/api/publication/31625361 ID - 31625361 LA - English DB - MTMT ER - TY - JOUR AU - Horváth, Ádám AU - Biró-Sütő, Tünde AU - Kántás, Boglárka AU - Payrits, Maja AU - Skodáné Földes, Rita AU - Szánti-Pintér, Eszter AU - Helyes, Zsuzsanna AU - Szőke, Éva TI - Antinociceptive Effects of Lipid Raft Disruptors, a Novel Carboxamido-Steroid and Methyl β-Cyclodextrin, in Mice by Inhibiting Transient Receptor Potential Vanilloid 1 and Ankyrin 1 Channel Activation JF - FRONTIERS IN PHYSIOLOGY J2 - FRONT PHYSIOL VL - 11 PY - 2020 PG - 9 SN - 1664-042X DO - 10.3389/fphys.2020.559109 UR - https://m2.mtmt.hu/api/publication/31608849 ID - 31608849 N1 - * Megosztott szerzőség LA - English DB - MTMT ER - TY - JOUR AU - Payrits, Maja AU - Horváth, Ádám AU - Biró-Sütő, Tünde AU - Erostyák, János AU - Makkai, Géza AU - Sághy, Éva AU - Pohóczky, Krisztina AU - Kecskés, Angéla AU - Kecskés, Miklós AU - Szolcsányi, János AU - Helyes, Zsuzsanna AU - Szőke, Éva TI - Resolvin D1 and D2 inhibit transient receptor potential vanilloid 1 and ankyrin 1 ion channel activation on sensory neurons via lipid raft modification JF - INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES J2 - INT J MOL SCI VL - 21 PY - 2020 IS - 14 PG - 17 SN - 1661-6596 DO - 10.3390/ijms21145019 UR - https://m2.mtmt.hu/api/publication/31387590 ID - 31387590 N1 - Funding Agency and Grant Number: National Brain Research Program [2017-1.2.1-NKP-2017-00002]; Hungarian Government [GINOP-2.3.2-15-2016-00050, EFOP-3.6.2-16-2017-00006, EFOP-3.6.2-16-2017-00008]; Janos Bolyai Research Scholarship of the Hungarian Academy of Sciences; University of Pecs [17886-4/23018/FEKUTSTRAT]; New National Excellence Program of the ministry of Human Capacities [UNKP-18-4]; New National Excellence Program of the ministry for Innovation and Technology [UNKP-19-4] Funding text: This work was supported by the National Brain Research Program 2017-1.2.1-NKP-2017-00002 (NAP-2; Chronic Pain Research Group). We acknowledge the grant of the Hungarian Government (GINOP-2.3.2-15-2016-00050, EFOP-3.6.2-16-2017-00006 and EFOP-3.6.2-16-2017-00008). E. Szoke A. Kecskes and E. Saghy were supported by the Janos Bolyai Research Scholarship of the Hungarian Academy of Sciences. The University of Pecs is acknowledged for a support by the 17886-4/23018/FEKUTSTRAT excellence grant. M. Payrits was supported by the New National Excellence Program of the ministry of Human Capacities UNKP-18-4. E. Szoke and E. Saghy were supported by the New National Excellence Program of the ministry of Human Capacities UNKP-18-4 and New National Excellence Program of the ministry for Innovation and Technology UNKP-19-4 grant. AB - Transient Receptor Potential Vanilloid 1 and Ankyrin 1 (TRPV1, TRPA1) cation channels are expressed in nociceptive primary sensory neurons and regulate nociceptor and inflammatory functions. Resolvins are endogenous lipid mediators. Resolvin D1 (RvD1) is described as a selective inhibitor of TRPA1-related postoperative and inflammatory pain in mice acting on the G protein-coupled receptor DRV1/GPR32. Resolvin D2 (RvD2) is a very potent TRPV1 and TRPA1 inhibitor in DRG neurons, and decreases inflammatory pain in mice acting on the GPR18 receptor, via TRPV1/TRPA1-independent mechanisms. We provided evidence that resolvins inhibited neuropeptide release from the stimulated sensory nerve terminals by TRPV1 and TRPA1 activators capsaicin (CAPS) and allyl-isothiocyanate (AITC), respectively. We showed that RvD1 and RvD2 in nanomolar concentrations significantly decreased TRPV1 and TRPA1 activation on sensory neurons by fluorescent calcium imaging and inhibited the CAPS-and AITC-evoked45Ca-uptake on TRPV1-and TRPA1-expressing CHO cells. Since CHO cells are unlikely to express resolvin receptors, resolvins are suggested to inhibit channel opening through surrounding lipid raft disruption. Here, we proved the ability of resolvins to alter the membrane polarity related to cholesterol composition by fluorescence spectroscopy. It is concluded that targeting lipid raft integrity can open novel peripheral analgesic opportunities by decreasing the activation of nociceptors. © 2020 by the authors. Licensee MDPI, Basel, Switzerland. LA - English DB - MTMT ER -