@article{MTMT:33543493,
	title = {Prolactin-releasing peptide contributes to stress-related mood disorders and inhibits sleep/mood regulatory melanin-concentrating hormone neurons in rats.},
	url = {https://m2.mtmt.hu/api/publication/33543493},
	author = {Vas, Szilvia and Papp, Rege Sugárka and Könczöl, Katalin and Bogáthy, Emese and Papp, Noémi and Ádori, Csaba and Durst, Máté and Sípos, Klaudia and Ocskay, Klementina and Farkas, Imre and Bálint, Flóra and Ferenczi, Szilamér and Török, Bibiána and Kovács, Anita and Szabó, Evelin and Zelena, Dóra and Kovács, Krisztina and Földes, Anna and Kató, Erzsébet and Köles, László and Bagdy, György and Palkovits, Miklós and Tóth, Zsuzsanna},
	doi = {10.1523/JNEUROSCI.2139-21.2022},
	journal-iso = {J NEUROSCI},
	journal = {JOURNAL OF NEUROSCIENCE},
	volume = {43},
	unique-id = {33543493},
	issn = {0270-6474},
	abstract = {Stress disorders impair sleep, quality of life, however, their pathomechanisms are unknown. Prolactin-releasing peptide (PrRP) is a stress mediator, therefore, we hypothesised that PrRP may be involved in the development of stress disorders. PrRP is produced by the medullary A1/A2 noradrenaline (NA) cells, which transmit stress signals to forebrain centers, and by non-NA cells in the hypothalamic dorsomedial nucleus. We found in male rats that both PrRP and PrRP-NA cells innervate melanin-concentrating hormone (MCH) producing neurons in the dorsolateral hypothalamus (DLH). These cells serve as a key hub for regulating sleep and affective states. Ex vivo, PrRP hyperpolarized MCH neurons and further increased the hyperpolarization caused by NA. Following sleep deprivation, intracerebroventricular PrRP injection reduced the number of REM sleep-active MCH cells. PrRP expression in the dorsomedial nucleus was up-regulated by sleep deprivation, while down-regulated by REM sleep rebound. Both in learned helplessness paradigm and after peripheral inflammation, impaired coping with sustained stress was associated with (i) overactivation of PrRP cells, (ii) PrRP protein and receptor depletion in the DLH, and (iii) dysregulation of MCH expression. Exposure to stress in PrRP insensitive period led to increased passive coping with stress. Normal PrRP signaling, therefore, seems to protect animals against stress-related disorders. PrRP signaling in the DLH is important component of the PrRP's action, which may be mediated by MCH neurons. Moreover, PrRP receptors were downregulated in the DLH of human suicidal victims. As stress-related mental disorders are the leading cause of suicide, our findings may have particular translational relevance.SIGNIFICANCE STATEMENT:Treatment resistance to monoaminergic antidepressants is a major problem. Neuropeptides that modulate the central monoaminergic signaling are promising targets for developing alternative therapeutic strategies. We found that stress-responsive prolactin-releasing peptide (PrRP) cells innervated melanin-concentrating hormone (MCH) neurons that are crucial in the regulation of sleep and mood. PrRP inhibited MCH cell activity and enhanced the inhibitory effect evoked by noradrenaline, a classic monoamine, on MCH neurons. We observed that impaired PrRP signaling led to failure in coping with chronic/repeated stress and was associated with altered MCH expression. We found alterations of the PrRP system also in suicidal human subjects. PrRP dysfunction may underlie stress disorders, and fine-tuning MCH activity by PrRP may be an important part of the mechanism.},
	year = {2023},
	eissn = {1529-2401},
	pages = {846-862},
	orcid-numbers = {Vas, Szilvia/0000-0001-7236-5672; Papp, Rege Sugárka/0000-0002-4720-0291; Bogáthy, Emese/0000-0003-3676-1170; Papp, Noémi/0000-0001-9460-9391; Durst, Máté/0000-0002-6456-4740; Sípos, Klaudia/0000-0003-0534-7348; Ocskay, Klementina/0000-0001-5848-2506; Farkas, Imre/0000-0002-0159-4408; Földes, Anna/0000-0002-4182-7886; Kató, Erzsébet/0000-0001-5786-0405; Köles, László/0000-0001-6708-0269; Bagdy, György/0000-0001-8141-3410; Palkovits, Miklós/0000-0003-0578-0387; Tóth, Zsuzsanna/0000-0002-0628-1320}
}

@article{MTMT:34139029,
	title = {Digitális távoktatás a COVID-19-járvány árnyékában – összhangban az orvosképzés megújulásával és modernizálásával a Semmelweis Egyetem Farmakológiai és Farmakoterápiás Intézetében},
	url = {https://m2.mtmt.hu/api/publication/34139029},
	author = {Köles, László and Riba, Pál and Al-Khrasani, Mahmoud and Brenner, Gábor and Giricz, Zoltán and Görbe, Anikó and Kató, Erzsébet and Király, Kornél P and Miklya, Ildikó and Varga, Zoltán and Zádori, Zoltán Sándor and Ferdinandy, Péter},
	journal-iso = {ORVOSKÉPZÉS},
	journal = {ORVOSKÉPZÉS},
	volume = {96},
	unique-id = {34139029},
	issn = {0030-6037},
	year = {2021},
	pages = {261-264},
	orcid-numbers = {Köles, László/0000-0001-6708-0269; Riba, Pál/0000-0002-7886-4816; Al-Khrasani, Mahmoud/0000-0001-8488-3266; Brenner, Gábor/0000-0001-7886-2960; Giricz, Zoltán/0000-0003-2036-8665; Görbe, Anikó/0000-0003-4908-1094; Kató, Erzsébet/0000-0001-5786-0405; Király, Kornél P/0000-0002-7252-0422; Miklya, Ildikó/0000-0003-0071-9026; Varga, Zoltán/0000-0002-2758-0784; Zádori, Zoltán Sándor/0000-0001-7312-618X; Ferdinandy, Péter/0000-0002-6424-6806}
}

@article{MTMT:31981561,
	title = {Trpm7-mediated calcium transport in hat-7 ameloblasts},
	url = {https://m2.mtmt.hu/api/publication/31981561},
	author = {Kádár, Kristóf György and Juhász, Viktória Orsolya and Földes, Anna and Rácz, Róbert and Zhang, Y. and Löchli, H. and Kató, Erzsébet and Köles, László and Steward, Martin Charles and Denbesten, P. and Varga, Gábor and Zsembery, Ákos},
	doi = {10.3390/ijms22083992},
	journal-iso = {INT J MOL SCI},
	journal = {INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES},
	volume = {22},
	unique-id = {31981561},
	issn = {1661-6596},
	abstract = {TRPM7 plays an important role in cellular Ca2+, Zn2+ and Mg2+ homeostasis. TRPM7 channels are abundantly expressed in ameloblasts and, in the absence of TRPM7, dental enamel is hypomineralized. The potential role of TRPM7 channels in Ca2+ transport during amelogenesis was investigated in the HAT-7 rat ameloblast cell line. The cells showed strong TRPM7 mRNA and protein expression. Characteristic TRPM7 transmembrane currents were observed, which increased in the absence of intracellular Mg2+ ([Mg2+]i ), were reduced by elevated [Mg2+]i, and were inhibited by the TRPM7 inhibitors NS8593 and FTY720. Mibefradil evoked similar currents, which were suppressed by elevated [Mg2+]i, reducing extracellular pH stimulated transmembrane currents, which were inhibited by FTY720. Naltriben and mibefradil both evoked Ca2+ influx, which was further enhanced by the acidic intracellular conditions. The SOCE inhibitor BTP2 blocked Ca2+ entry induced by naltriben but not by mibefradil. Thus, in HAT-7 cells, TRPM7 may serves both as a potential modulator of Orai-dependent Ca2+ uptake and as an independent Ca2+ entry pathway sensitive to pH. Therefore, TRPM7 may contribute directly to transepithelial Ca2+ transport in amelogenesis. © 2021 by the authors. Licensee MDPI, Basel, Switzerland.},
	keywords = {PH; MAGNESIUM; enamel; Amelogenesis; Calcium entry; store-operated calcium entry; TRPM7 channel protein},
	year = {2021},
	eissn = {1422-0067},
	orcid-numbers = {Kádár, Kristóf György/0000-0002-7164-7827; Földes, Anna/0000-0002-4182-7886; Rácz, Róbert/0000-0002-6341-4839; Kató, Erzsébet/0000-0001-5786-0405; Köles, László/0000-0001-6708-0269; Varga, Gábor/0000-0002-5506-8198; Zsembery, Ákos/0000-0003-0253-9379}
}

@{MTMT:31611024,
	title = {Féreg- és rovarellenes szerek},
	url = {https://m2.mtmt.hu/api/publication/31611024},
	author = {Szalka, András and Kató, Erzsébet},
	booktitle = {Farmakológia és klinikai farmakológia},
	unique-id = {31611024},
	year = {2020},
	pages = {848-853},
	orcid-numbers = {Kató, Erzsébet/0000-0001-5786-0405}
}

@{MTMT:31611021,
	title = {Protozoonellenes szerek},
	url = {https://m2.mtmt.hu/api/publication/31611021},
	author = {Szalka, András and Kató, Erzsébet},
	booktitle = {Farmakológia és klinikai farmakológia},
	unique-id = {31611021},
	year = {2020},
	pages = {839-847},
	orcid-numbers = {Kató, Erzsébet/0000-0001-5786-0405}
}

@{MTMT:31610813,
	title = {A véralvadást befolyásoló szerek},
	url = {https://m2.mtmt.hu/api/publication/31610813},
	author = {Köles, László and Kató, Erzsébet},
	booktitle = {Farmakológia és klinikai farmakológia},
	unique-id = {31610813},
	year = {2020},
	pages = {545-559},
	orcid-numbers = {Köles, László/0000-0001-6708-0269; Kató, Erzsébet/0000-0001-5786-0405}
}

@article{MTMT:3143505,
	title = {The role of P2X7 receptors in a rodent PCP-induced schizophrenia model},
	url = {https://m2.mtmt.hu/api/publication/3143505},
	author = {Koványi, Bence and Csölle, Cecília and Calovi, Stefano and Hanuska, Adrienn and Kató, Erzsébet and Köles, László and Bhattacharya, A and Haller, József and Sperlágh, Beáta},
	doi = {10.1038/srep36680},
	journal-iso = {SCI REP},
	journal = {SCIENTIFIC REPORTS},
	volume = {6},
	unique-id = {3143505},
	issn = {2045-2322},
	abstract = {P2X7 receptors (P2X7Rs) are ligand-gated ion channels sensitive to extracellular ATP. Here we examined for the first time the role of P2X7R in an animal model of schizophrenia. Using the PCP induced schizophrenia model we show that both genetic deletion and pharmacological inhibition of P2X7Rs alleviate schizophrenia-like behavioral alterations. In P2rx7+/+ mice, PCP induced hyperlocomotion, stereotype behavior, ataxia and social withdrawal. In P2X7 receptor deficient mice (P2rx7-/-), the social interactions were increased, whereas the PCP induced hyperlocomotion and stereotype behavior were alleviated. The selective P2X7 receptor antagonist JNJ-47965567 partly replicated the effect of gene deficiency on PCP-induced behavioral changes and counteracted PCP-induced social withdrawal. We also show that PCP treatment upregulates and increases the functional responsiveness of P2X7Rs in the prefrontal cortex of young adult animals. The amplitude of NMDA evoked currents recorded from layer V pyramidal neurons of cortical slices were slightly decreased by both genetic deletion of P2rx7 and by JNJ-47965567. PCP induced alterations in mRNA expression encoding schizophrenia-related genes, such as NR2A, NR2B, neuregulin 1, NR1 and GABA alpha1 subunit were absent in the PFC of young adult P2rx7-/- animals. Our findings point to P2X7R as a potential therapeutic target in schizophrenia.},
	year = {2016},
	eissn = {2045-2322},
	orcid-numbers = {Hanuska, Adrienn/0000-0002-5031-9250; Kató, Erzsébet/0000-0001-5786-0405; Köles, László/0000-0001-6708-0269; Haller, József/0000-0003-4315-3026}
}

@article{MTMT:2981932,
	title = {Modulation of excitatory neurotransmission by neuronal/glial signalling molecules: interplay between purinergic and glutamatergic systems},
	url = {https://m2.mtmt.hu/api/publication/2981932},
	author = {Köles, László and Kató, Erzsébet and Hanuska, Adrienn and Zádori, Zoltán Sándor and Al-Khrasani, Mahmoud and Zelles, Tibor and Rubini, P and Illes, P},
	doi = {10.1007/s11302-015-9480-5},
	journal-iso = {PURINERG SIGNAL},
	journal = {PURINERGIC SIGNALLING},
	volume = {12},
	unique-id = {2981932},
	issn = {1573-9538},
	year = {2016},
	eissn = {1573-9546},
	pages = {1-24},
	orcid-numbers = {Köles, László/0000-0001-6708-0269; Kató, Erzsébet/0000-0001-5786-0405; Hanuska, Adrienn/0000-0002-5031-9250; Zádori, Zoltán Sándor/0000-0001-7312-618X; Al-Khrasani, Mahmoud/0000-0001-8488-3266; Zelles, Tibor/0000-0002-0357-0469}
}

@article{MTMT:2951337,
	title = {A new potent analgesic agent with reduced liability to produce morphine tolerance},
	url = {https://m2.mtmt.hu/api/publication/2951337},
	author = {Király, Kornél P and Caputi, FF and Hanuska, Adrienn and Kató, Erzsébet and Balogh, Mihály and Köles, László and Palmisano, M and Riba, Pál and Hosztafi, Sándor and Romualdi, P and Candeletti, S and Ferdinandy, Péter and Fürst, Zsuzsanna and Al-Khrasani, Mahmoud},
	doi = {10.1016/j.brainresbull.2015.07.005},
	journal-iso = {BRAIN RES BULL},
	journal = {BRAIN RESEARCH BULLETIN},
	volume = {117},
	unique-id = {2951337},
	issn = {0361-9230},
	abstract = {The therapeutic use of opioids is limited by the development of tolerance to the analgesic effect and the cellular and molecular mechanisms underlying this phenomenon are still not completely understood. For this reason the search for new analgesic derivatives, endowed with lower tolerance, is always an active field. The newly synthesized 14-. O-Methylmorphine-6-sulfate (14-. O-MeM6SU) shows high efficacy in in vitro assays and a strong analgesic action in the rat tail flick test. The aim of present work was to investigate: the analgesic effect of 14-. O-MeM6SU in mouse tail-flick test; the tolerance to analgesic effect of 14-. O-MeM6SU compared to morphine in mice, the effects of test compounds on glutamatergic neurotransmission by measuring spontaneous excitatory postsynaptic currents (sEPSCs) of layer V pyramidal cells from rat prefrontal cortices; and the effect of acute and chronic 14-. O-MeM6SU treatments on opioid receptor gene expression in SH-SY5Y neuroblastoma cells expressing μ-opioid (MOP) and nociceptin/opioid receptor-like 1 (NOP) receptors.14-O-MeM6SU was 17 times more potent than morphine in analgesia and had long duration of action in analgesic dose equipotent to morphine. Mice were treated subcutaneously (s.c.) either with 200μmol/kg morphine or with 14-O-MeM6SU (12μmol/kg) twice daily for three days. The magnitude of tolerance or cross-tolerance indicated by the shift in antinociceptive ED<inf>50</inf> measured was greater for morphine compared to 14-O-MeM6SU. Subsequent to behavioral testing, patch-clamp experiments in layer V pyramidal neurons of rat prefrontal cortical slices in the presence of bicuculline were performed. Both 14-O-MeM6SU (0.1μM) and morphine (1μM) decreased the frequency of sEPSCs, indicating reduction of glutamate release. The effect of the novel compound was reversed by the opioid receptor antagonist naloxone, indicating an opioid mediated action. In contrast, the amplitude was not affected. Finally, gene expression data showed a dose dependent down-regulation of MOP receptor after 24h and 48h exposure to 14-O-MeM6SU. Interestingly, no changes were detected for NOP receptor gene expression. The specific lack of this effect could be related to the lower tolerance development to analgesic effect of 14-O-MeM6SU. Furthermore, 14-O-MeM6SU displayed high intrinsic efficacy possibly an important factor in the observed effects. Further, the observed inhibition of glutamatergic signaling might be attributed also to the reduction of opioid tolerance. Based on our results the development of a new clinically important, safe analgesic agent might be possible. © 2015 Elsevier Inc.},
	keywords = {Male; prefrontal cortex; ARTICLE; TOLERANCE; MORPHINE; ANALGESIA; MOUSE; human; OPIATE RECEPTOR; priority journal; controlled study; nonhuman; dose response; animal model; animal experiment; animal cell; in vitro study; excitatory postsynaptic potential; neurotransmission; glutamic acid; Gene Expression; human cell; analgesic agent; unclassified drug; drug efficacy; tissue injury; naloxone; down regulation; pyramidal nerve cell; analgesic activity; mu opiate receptor; drug potency; opiate antagonist; Glutamatergic synapse; neuroblastoma cell; tissue slice; cross tolerance; antinociceptive agent; bicuculline; tail flick test; morphine tolerance; glutamatergic transmission; patch clamp technique; experimental behavioral test; 14 o methylmorphine 6 sulfate; MOP receptor down-regulation; 14-O-Methylmorphine-6-sulfate},
	year = {2015},
	eissn = {1873-2747},
	pages = {32-38},
	orcid-numbers = {Király, Kornél P/0000-0002-7252-0422; Hanuska, Adrienn/0000-0002-5031-9250; Kató, Erzsébet/0000-0001-5786-0405; Balogh, Mihály/0000-0003-3296-0316; Köles, László/0000-0001-6708-0269; Riba, Pál/0000-0002-7886-4816; Hosztafi, Sándor/0000-0003-3793-4651; Ferdinandy, Péter/0000-0002-6424-6806; Fürst, Zsuzsanna/0000-0002-2760-1274; Al-Khrasani, Mahmoud/0000-0001-8488-3266}
}

@article{MTMT:2603498,
	title = {Astrocyte-neuron interaction in the substantia gelatinosa of the spinal cord dorsal horn via P2X7 receptor-mediated release of glutamate and reactive oxygen species.},
	url = {https://m2.mtmt.hu/api/publication/2603498},
	author = {Ficker, C and Kovács-Rozmer, Katalin and Kató, Erzsébet and Andó, Rómeó and Schumann, L and Krügel, U and Franke, H and Sperlágh, Beáta and Riedel, T and Illes, P},
	doi = {10.1002/glia.22707},
	journal-iso = {GLIA},
	journal = {GLIA},
	volume = {62},
	unique-id = {2603498},
	issn = {0894-1491},
	year = {2014},
	eissn = {1098-1136},
	pages = {1671-1686},
	orcid-numbers = {Kató, Erzsébet/0000-0001-5786-0405}
}