@article{MTMT:30336483,
	title = {Potential role of the ecto-5 '-nucleotidase in morphine -induced uridine release and neurobehavioral changes},
	url = {https://m2.mtmt.hu/api/publication/30336483},
	author = {Che, Xiaohang and Liu, Ping and Wu, Chunfu and Song, Wu and An, Nina and Yu, Lisha and Bai, Yijun and Xing, Zheng and Cai, Jialing and Wang, Xiaomin and Yang, Jingyu},
	doi = {10.1016/j.neuropharm.2018.07.035},
	journal-iso = {NEUROPHARMACOLOGY},
	journal = {NEUROPHARMACOLOGY},
	volume = {141},
	unique-id = {30336483},
	issn = {0028-3908},
	abstract = {There is growing evidence that uridine may act as an endogenous neuromodulator with a potential signaling role in the central nervous system in addition to its function in pyrimidine metabolism. We previously found that acute morphine treatment significantly increased uridine release in the dorsal striatum of mice, indicating that uridine may contribute to morphine-induced neurobehavioral changes. In the present study, we analyzed the mechanism involved in morphine-induced uridine release and the role of uridine in morphine-induced neurobehavioral changes. Uridine release in the dorsal striatum of mice was assessed by in vivo microdialysis coupled with high performance liquid chromatography (HPLC) after morphine treatment. Western blotting and immunofluorescence were used to evaluate the expression of uridine-related proteins. Morphine-induced neurobehavioral changes were assessed by locomotor activity, behavioral sensitization and conditioned place preference (CPP) test. The expression of NT5E, an extracellular enzyme involved in formation of nucleosides, including uridine, was specifically knocked down in the dorsal striatum of mice using adeno-associated virus (AAV)-mediated short hairpin RNA (shRNA). The results indicated that both acute and chronic morphine administration significantly increased uridine release in the dorsal striatum, and this was associated with upregulation of NT5E but not other uridine-related proteins. Inhibition of NT5E with APCP or shRNA markedly inhibited morphine-induced uridine release in the dorsal striatum and related neurobehavioral changes, including hyperlocomotor activity, behavioral sensitization and CPP. Our data give a better understanding of the contribution of NT5E to morphine-induced uridine release and neurobehavioral changes, and identify NT5E as a potential target for treating morphine abuse.},
	keywords = {MORPHINE; uridine; NEUROBEHAVIORAL CHANGES; Ecto-5 '-nucleotidases},
	year = {2018},
	eissn = {1873-7064},
	pages = {1-10}
}

@article{MTMT:30336484,
	title = {Intracerebral microdialysis of adenosine and adenosine monophosphate - a systematic review and meta-regression analysis of baseline concentrations},
	url = {https://m2.mtmt.hu/api/publication/30336484},
	author = {van der Mierden, Stevie and Savelyev, Sergey A. and IntHout, Joanna and de Vries, Rob B. M. and Leenaars, Cathalijn H. C.},
	doi = {10.1111/jnc.14552},
	journal-iso = {J NEUROCHEM},
	journal = {JOURNAL OF NEUROCHEMISTRY},
	volume = {147},
	unique-id = {30336484},
	issn = {0022-3042},
	abstract = {Microdialysis is a method to study the extracellular space invivo, based on the principle of diffusion. It can be used to measure various small molecules including the neuroregulator adenosine. Baseline levels of the compounds measured with microdialysis vary over studies. We systematically reviewed the literature to investigate the full range of reported baseline concentrations of adenosine and adenosine monophosphate in microdialysates. We performed a meta-regression analysis to study the influence of flow rate, probe membrane surface area, species, brain area and anaesthesia versus freely behaving, on the adenosine concentration. Baseline adenosine concentrations in microdialysates ranged from 0.8 to 2100nM. There was limited evidence on baseline adenosine monophosphate concentrations in microdialysates. Across studies, we found effects of flow rate and anaesthesia versus freely behaving on dialysate adenosine concentrations (p0.001), but not of probe membrane surface, species, or brain area (p0.14). With increasing flow rate, adenosine concentrations decreased. With anaesthesia, adenosine concentrations increased. The effect of other predictor variables on baseline adenosine concentrations, for example, post-surgical recovery time, could not be analysed because of a lack of reported data. This study shows that meta-regression can be used as an alternative to new animal experiments to answer research questions in the field of neurochemistry. However, current levels of reporting of primary studies are insufficient to reach the full potential of this approach; 63 out of 133 studies could not be included in the analysis because of insufficient reporting, and several potentially relevant factors had to be excluded from the analyses. The level of reporting of experimental detail needs to improve.},
	keywords = {Meta-analysis; adenosine; MICRODIALYSIS; Systematic literature review},
	year = {2018},
	eissn = {1471-4159},
	pages = {58-70},
	orcid-numbers = {van der Mierden, Stevie/0000-0001-7080-1872}
}

@article{MTMT:2904124,
	title = {Absence epileptic activity changing effects of non-adenosine nucleoside inosine, guanosine and uridine in Wistar Albino Glaxo Rijswijk rats.},
	url = {https://m2.mtmt.hu/api/publication/2904124},
	author = {Kovács, Zsolt and Kékesi, Adrienna Katalin and Dobolyi, Árpád and Lakatos, Renáta Krisztina and Juhász, Gábor Dénes},
	doi = {10.1016/j.neuroscience.2015.05.054},
	journal-iso = {NEUROSCIENCE},
	journal = {NEUROSCIENCE},
	volume = {300},
	unique-id = {2904124},
	issn = {0306-4522},
	abstract = {Adenosine (Ado) and non-adenosine (non-Ado) nucleosides such as inosine (Ino), guanosine (Guo) and uridine (Urd) may have regionally different roles in the regulation of physiological and pathophysiological processes in the central nervous system (CNS) such as epilepsy. It was demonstrated previously that Ino and Guo decreased quinolinic acid (QA)-induced seizures and Urd reduced penicillin-, bicuculline- and pentylenetetrazole (PTZ)-induced seizures. It has also been demonstrated that Ino and Urd may exert their effects through GABAergic system by altering the function of GABAA type of gamma-aminobutyric acid receptors (GABAA receptors) whereas Guo decreases glutamate-induced excitability through glutamatergic system, which systems (GABAergic and glutamatergic) are involved in pathomechanisms of absence epilepsy. Thus, we hypothesized that Ino and Guo, similarly to the previously described effect of Urd, might also decrease absence epileptic activity. We investigated in the present study whether intraperitoneal (i.p.) application of Ino (500 and 1000mg/kg), Guo (20 and 50mg/kg), Urd (500 and 1000mg/kg), GABAA receptor agonist muscimol (1 and 3mg/kg), GABAA receptor antagonist bicuculline (2 and 4mg/kg), non-selective Ado receptor antagonist theophylline (5 and 10mg/kg) and non-competitive N-methyl-d-aspartate (NMDA) receptor antagonist (+)-5-methyl-10,11-dihydro-5H-dibenzo (a,d) cyclohepten-5,10-imine maleate (MK-801, 0.0625 and 0.1250mg/kg) alone and in combination have modulatory effects on absence epileptic activity in Wistar Albino Glaxo Rijswijk (WAG/Rij) rats. We found that Guo decreased the number of spike-wave discharges (SWDs) whereas Ino increased it dose-dependently. We strengthened that Urd can decrease absence epileptic activity. Our results suggest that Guo, Urd and their analogs could be potentially effective drugs for treatment of human absence epilepsy.},
	year = {2015},
	eissn = {1873-7544},
	pages = {593-608},
	orcid-numbers = {Kovács, Zsolt/0000-0001-8571-5686; Kékesi, Adrienna Katalin/0000-0003-3042-4878; Dobolyi, Árpád/0000-0003-0397-2991; Juhász, Gábor Dénes/0000-0002-0849-6931}
}

@article{MTMT:2790273,
	title = {Non-adenosine Nucleoside Inosine, Guanosine and Uridine as Promising Antiepileptic Drugs: a Summary of Current Literature.},
	url = {https://m2.mtmt.hu/api/publication/2790273},
	author = {Kovács, Zsolt and Kékesi, Adrienna Katalin and Juhász, Gábor Dénes and Barna, János and Héja, László and Lakatos, Renáta Krisztina and Dobolyi, Árpád},
	doi = {10.2174/1389557514666141107120226},
	journal-iso = {MINI REV MED CHEM},
	journal = {MINI-REVIEWS IN MEDICINAL CHEMISTRY},
	volume = {14},
	unique-id = {2790273},
	issn = {1389-5575},
	abstract = {Adenosine (Ado) and some non-adenosine (non-Ado) nucleosides including inosine (Ino), guanosine (Guo) and uridine (Urd) are modulatory molecules in the central nervous system (CNS), regulating different physiological and pathophysiological processes in the brain such as sleep and epilepsy. Indeed, different drugs effective on adenosinergic system (e.g., Ado metabolism inhibitors, agonists and antagonists of Ado receptors) are being used in drug development for the treatment of epileptic disorders. Although (i) endogenous Ino, Guo and Urd showed anticonvulsant/antiepileptic effects (e.g., in quinolinic acid - induced seizures and in different epilepsy models such as hippocampal kindling models), and (ii) there is need to generate new and more effective antiepileptic drugs for the treatment of drug-resistant epilepsies, our knowledge about antiepileptic influence of non-Ado nucleosides is far from complete. Thus, in this review article, we give a short summary of anticonvulsant/antiepileptic effects and mechanisms evoked by Ino, Guo, and Urd. Finally, we discuss some non-Ado nucleoside derivatives and their structures, which may be candidates as potential antiepileptic agents.},
	year = {2014},
	eissn = {1875-5607},
	pages = {1033-1042},
	orcid-numbers = {Kovács, Zsolt/0000-0001-8571-5686; Kékesi, Adrienna Katalin/0000-0003-3042-4878; Juhász, Gábor Dénes/0000-0002-0849-6931; Barna, János/0000-0002-4394-2175; Dobolyi, Árpád/0000-0003-0397-2991}
}

@article{MTMT:2374138,
	title = {The Antiepileptic Potential of Nucleosides},
	url = {https://m2.mtmt.hu/api/publication/2374138},
	author = {Kovács, Zsolt and Kékesi, Adrienna Katalin and Juhász, Gábor Dénes and Dobolyi, Árpád},
	doi = {10.2174/1381612819666131119154505},
	journal-iso = {CURR MED CHEM},
	journal = {CURRENT MEDICINAL CHEMISTRY},
	volume = {21},
	unique-id = {2374138},
	issn = {0929-8673},
	year = {2014},
	eissn = {1875-533X},
	pages = {788-821},
	orcid-numbers = {Kovács, Zsolt/0000-0001-8571-5686; Kékesi, Adrienna Katalin/0000-0003-3042-4878; Juhász, Gábor Dénes/0000-0002-0849-6931; Dobolyi, Árpád/0000-0003-0397-2991}
}

@inbook{MTMT:1772574,
	title = {Anatomical Distribution of Nucleoside System in the Human Brain and Implications for Therapy},
	url = {https://m2.mtmt.hu/api/publication/1772574},
	author = {Kovács, Zsolt and Dobolyi, Árpád},
	booktitle = {Adenosine: A Key Link between Metabolism and Brain Activity},
	doi = {10.1007/978-1-4614-3903-5_29},
	unique-id = {1772574},
	year = {2013},
	pages = {621-656},
	orcid-numbers = {Kovács, Zsolt/0000-0001-8571-5686; Dobolyi, Árpád/0000-0003-0397-2991}
}

@article{MTMT:2360733,
	title = {5'-nucleotidases, nucleosides and their distribution in the brain: pathological and therapeutic implications},
	url = {https://m2.mtmt.hu/api/publication/2360733},
	author = {Kovács, Zsolt and Dobolyi, Árpád and Kékesi, Adrienna Katalin and Juhász, Gábor Dénes},
	doi = {10.2174/0929867311320340003},
	journal-iso = {CURR MED CHEM},
	journal = {CURRENT MEDICINAL CHEMISTRY},
	volume = {20},
	unique-id = {2360733},
	issn = {0929-8673},
	year = {2013},
	eissn = {1875-533X},
	pages = {4217-4240},
	orcid-numbers = {Kovács, Zsolt/0000-0001-8571-5686; Dobolyi, Árpád/0000-0003-0397-2991; Kékesi, Adrienna Katalin/0000-0003-3042-4878; Juhász, Gábor Dénes/0000-0002-0849-6931}
}

@article{MTMT:2335390,
	title = {Uridine modulates neuronal activity and inhibits spike-wave discharges of absence epileptic Long Evans and Wistar Albino Glaxo/Rijswijk rats},
	url = {https://m2.mtmt.hu/api/publication/2335390},
	author = {Kovács, Zsolt and Slézia, Andrea and Bali, Zsolt Kristóf and Kovács, Péter and Dobolyi, Árpád and Szikra, Tamás and Hernádi, István and Juhász, Gábor Dénes},
	doi = {10.1016/j.brainresbull.2013.05.009},
	journal-iso = {BRAIN RES BULL},
	journal = {BRAIN RESEARCH BULLETIN},
	volume = {97},
	unique-id = {2335390},
	issn = {0361-9230},
	keywords = {EEG; pyrimidine nucleoside; Spike-wave discharges; Extracellular neuronal activity; Multibarrel microiontophoresis; Absence epileptic rats},
	year = {2013},
	eissn = {1873-2747},
	pages = {16-23},
	orcid-numbers = {Kovács, Zsolt/0000-0001-8571-5686; Slézia, Andrea/0000-0002-4528-3169; Bali, Zsolt Kristóf/0000-0003-0712-0788; Kovács, Péter/0000-0001-5732-7432; Dobolyi, Árpád/0000-0003-0397-2991; Hernádi, István/0000-0001-7882-4817; Juhász, Gábor Dénes/0000-0002-0849-6931}
}

@article{MTMT:22886405,
	title = {Characterization of basal and morphine-induced uridine release in the striatum: An in vivo microdialysis study in mice},
	url = {https://m2.mtmt.hu/api/publication/22886405},
	author = {Song, W and Wu, C-F and Liu, P and Xiang, R-W and Wang, F and Dong, Y-X and Yang, J-Y},
	doi = {10.1007/s11064-012-0903-1},
	journal-iso = {NEUROCHEM RES},
	journal = {NEUROCHEMICAL RESEARCH},
	volume = {38},
	unique-id = {22886405},
	issn = {0364-3190},
	year = {2013},
	eissn = {1573-6903},
	pages = {153-161}
}

@article{MTMT:1507582,
	title = {Uridine function in the central nervous system},
	url = {https://m2.mtmt.hu/api/publication/1507582},
	author = {Dobolyi, Árpád and Juhász, Gábor Dénes and Kovács, Zsolt and Kardos, Julianna},
	doi = {10.2174/156802611795347618},
	journal-iso = {CURR TOP MED CHEM},
	journal = {CURRENT TOPICS IN MEDICINAL CHEMISTRY},
	volume = {11},
	unique-id = {1507582},
	issn = {1568-0266},
	year = {2011},
	eissn = {1873-4294},
	pages = {1058-1067},
	orcid-numbers = {Dobolyi, Árpád/0000-0003-0397-2991; Juhász, Gábor Dénes/0000-0002-0849-6931; Kovács, Zsolt/0000-0001-8571-5686}
}

@article{MTMT:1445693,
	title = {Area, age and gender dependence of the nucleoside system in the brain: a review of current literature},
	url = {https://m2.mtmt.hu/api/publication/1445693},
	author = {Kovács, Zsolt and Juhász, Gábor Dénes and Palkovits, Miklós and Dobolyi, Árpád and Kékesi, Adrienna Katalin},
	doi = {10.2174/156802611795347636},
	journal-iso = {CURR TOP MED CHEM},
	journal = {CURRENT TOPICS IN MEDICINAL CHEMISTRY},
	volume = {11},
	unique-id = {1445693},
	issn = {1568-0266},
	keywords = {Animals; Age Factors; Female; Male; Humans; RABBITS; MICE; RATS; signal transduction; Organ Specificity; Sex Factors; Gene Expression; Brain/*metabolism; Biological Transport/physiology; Neurons/cytology/metabolism; Schizophrenia/metabolism/physiopathology; Receptors, Purinergic/genetics/*metabolism; Parkinson Disease/metabolism/physiopathology; Nucleosides/*metabolism; Nucleoside Transport Proteins/genetics/*metabolism; Neuroglia/cytology/metabolism; Metabolic Networks and Pathways/physiology; Alzheimer Disease/metabolism/physiopathology},
	year = {2011},
	eissn = {1873-4294},
	pages = {1012-1033},
	orcid-numbers = {Kovács, Zsolt/0000-0001-8571-5686; Juhász, Gábor Dénes/0000-0002-0849-6931; Palkovits, Miklós/0000-0003-0578-0387; Dobolyi, Árpád/0000-0003-0397-2991; Kékesi, Adrienna Katalin/0000-0003-3042-4878}
}

@article{MTMT:1482495,
	title = {The Role of Extracellular Adenosine in Chemical Neurotransmission in the Hippocampus and Basal Ganglia: Pharmacological and Clinical Aspects.},
	url = {https://m2.mtmt.hu/api/publication/1482495},
	author = {Sperlágh, Beáta and Vizi, E. Szilveszter},
	doi = {10.2174/156802611795347564},
	journal-iso = {CURR TOP MED CHEM},
	journal = {CURRENT TOPICS IN MEDICINAL CHEMISTRY},
	volume = {11},
	unique-id = {1482495},
	issn = {1568-0266},
	abstract = {Now there is general agreement that the purine nucleoside adenosine is an important neuromodulator in the central nervous system, playing a crucial role in neuronal excitability and synaptic/non-synaptic transmission in the hippocampus and basal ganglia. Adenosine is derived from the breakdown of extra- or intracellular ATP and is released upon a variety of physiological and pathological stimuli from neuronal and non-neuronal sources, i.e. from glial cells and exerts effects diffusing far away from release sites. The resultant elevation of adenosine levels in the extracellular space reaches micromolar level, and leads to the activation A(1), A(2A), A(2B) and A(3) receptors, localized to pre- and postsynaptic as well as extrasynaptic sites. Activation of presynaptic A(1) receptors inhibits the release of the majority of transmitters including glutamate, acetylcholine, noradrenaline, 5-HT and dopamine, whilst the stimulation of A(2A) receptors facilitates the release of glutamate and acetylcholine and inhibits the release of GABA. These actions underlie modulation of neuronal excitability, synaptic plasticity and coordination of neural networks and provide intriguing target sites for pharmacological intervention in ischemia and Parkinson's disease. However, despite that adenosine is also released during ischemia, A(1) adenosine receptors do not participate in the modulation of excitotoxic glutamate release, which is nonsynaptic and is due to the reverse operation of transporters. Instead, extrasynaptic A(1) receptors might be responsible for the neuroprotection afforded by A(1) receptor activation.},
	year = {2011},
	eissn = {1873-4294},
	pages = {1034-1046},
	orcid-numbers = {Vizi, E. Szilveszter/0000-0002-9557-4597}
}

@article{MTMT:1332491,
	title = {Gender- and age-dependent changes in nucleoside levels in the cerebral cortex and white matter of the human brain.},
	url = {https://m2.mtmt.hu/api/publication/1332491},
	author = {Kovács, Zsolt and Juhász, Gábor Dénes and Dobolyi, Árpád and Bobest, M and Papp, V and Takats, L and Kékesi, Adrienna Katalin},
	doi = {10.1016/j.brainresbull.2009.10.010},
	journal-iso = {BRAIN RES BULL},
	journal = {BRAIN RESEARCH BULLETIN},
	volume = {81},
	unique-id = {1332491},
	issn = {0361-9230},
	abstract = {Nucleosides are neuromodulators that participate in various neuronal functions in the brain. In previous studies, we described regional differences in the concentrations of nucleosides and their derivatives in the human brain. To better understand the functions of nucleosides in the central nervous system, we investigated gender- and age-dependent changes in the levels of nucleosides and their metabolites. The concentrations of uridine, inosine, guanosine and adenosine as well as uracil, hypoxanthine and xanthine were measured in the frontal cortex and white matter of post-mortem brain tissue samples of middle-aged and old men as well as women. The average in vivo concentrations calculated from the 40 samples investigated (regardless of anatomical locations, gender or age; mean +/- S.E.M.) were as follows (pmol/mg wet tissue weight): 9.7 +/- 0.8 adenosine, 85.8 +/- 3.9 inosine, 14.3 +/- 0.9 guanosine, 37.3 +/- 1.8 uridine, 8.9 +/- 0.6 uracil, 63.3 +/- 2.1 hypoxanthine and 38.7 +/- 1.5 xanthine. We conclude that concentration differences between uridine, inosine, guanosine and adenosine in the frontal cortex and cerebral white matter suggest that nucleoside metabolism is altered with aging and regulated differently between men and women.},
	year = {2010},
	eissn = {1873-2747},
	pages = {579-584},
	orcid-numbers = {Kovács, Zsolt/0000-0001-8571-5686; Juhász, Gábor Dénes/0000-0002-0849-6931; Dobolyi, Árpád/0000-0003-0397-2991; Kékesi, Adrienna Katalin/0000-0003-3042-4878}
}

@article{MTMT:1332490,
	title = {Nucleoside Map of the Human Central Nervous System},
	url = {https://m2.mtmt.hu/api/publication/1332490},
	author = {Kovács, Zsolt and Dobolyi, Árpád and Juhász, Gábor Dénes and Kékesi, Adrienna Katalin},
	doi = {10.1007/s11064-009-0080-z},
	journal-iso = {NEUROCHEM RES},
	journal = {NEUROCHEMICAL RESEARCH},
	volume = {35},
	unique-id = {1332490},
	issn = {0364-3190},
	abstract = {Nucleosides are neuromodulators that have a wide range of biological roles in the brain. In order to better understand the function of nucleosides in the human central nervous system (CNS), we constructed a nucleoside map showing the concentration of various nucleosides and their metabolites using post mortem samples from 61 human brain areas and 4 spinal cord areas. We evaluated in vivo tissue levels of four nucleosides (uridine, inosine, guanosine, and adenosine) and three of their metabolites (uracil, hypoxanthine, and xanthine). The concentrations of nucleosides were unevenly distributed across different brain regions, where the highest levels were found in the cerebral cortex and basal ganglia, whereas the lowest concentrations were located in the locus coeruleus, the zona incerta, the substantia nigra, and the inferior colliculus. The regional differences in nucleoside levels in the CNS may reflect the distinct physiological functions adopted by these compounds in different brain areas.},
	year = {2010},
	eissn = {1573-6903},
	pages = {452-464},
	orcid-numbers = {Kovács, Zsolt/0000-0001-8571-5686; Dobolyi, Árpád/0000-0003-0397-2991; Juhász, Gábor Dénes/0000-0002-0849-6931; Kékesi, Adrienna Katalin/0000-0003-3042-4878}
}

@{MTMT:21220568,
	title = {The Role of Purine and Pyrimidine Nucleosides in Snake Venoms},
	url = {https://m2.mtmt.hu/api/publication/21220568},
	author = {Aird, SD},
	booktitle = {Handbook of Venoms and Toxins of Reptiles},
	publisher = {CRC Press},
	unique-id = {21220568},
	year = {2009},
	pages = {393}
}

@article{MTMT:10091552,
	title = {Effect of uridine of presynaptic NMDA and kainate receptor of rat brain cortex},
	url = {https://m2.mtmt.hu/api/publication/10091552},
	author = {Petrova, LN and Gabrelian, AV},
	doi = {10.1007/s10517-008-0080-z},
	journal-iso = {B EXP BIOL MED+},
	journal = {BULLETIN OF EXPERIMENTAL BIOLOGY AND MEDICINE},
	volume = {145},
	unique-id = {10091552},
	issn = {0007-4888},
	year = {2008},
	eissn = {1573-8221},
	pages = {320-322}
}

@article{MTMT:21838385,
	title = {Effects of uridine on kindling},
	url = {https://m2.mtmt.hu/api/publication/21838385},
	author = {Zhao, Q and Shatskikh, T and Marolewski, A and Rusche, JR and Holmes, GL},
	doi = {10.1016/j.yebeh.2008.02.002},
	journal-iso = {EPILEPSY BEHAV},
	journal = {EPILEPSY & BEHAVIOR},
	volume = {13},
	unique-id = {21838385},
	issn = {1525-5050},
	year = {2008},
	eissn = {1525-5069},
	pages = {47-51}
}

@mastersthesis{MTMT:23161266,
	title = {Aktivitás-függő idegrendszeri plaszticitás fiziológiás és patológiás folyamatokban},
	url = {https://m2.mtmt.hu/api/publication/23161266},
	author = {Papp, Andrea Márta},
	unique-id = {23161266},
	year = {2007}
}

@article{MTMT:1138097,
	title = {Extracellular level of GABA and Glu: In vivo microdialysis-HPLC measurements},
	url = {https://m2.mtmt.hu/api/publication/1138097},
	author = {Nyitrai, Gabriella and Kékesi, Adrienna Katalin and Juhász, Gábor Dénes},
	doi = {10.2174/156802606777323674},
	journal-iso = {CURR TOP MED CHEM},
	journal = {CURRENT TOPICS IN MEDICINAL CHEMISTRY},
	volume = {6},
	unique-id = {1138097},
	issn = {1568-0266},
	abstract = {In spite of several studies showing specific physiological functions of changes in the extracellular level of the major excitatory and inhibitory transmitters, Glu and GABA within the brain ([Glu]EXT, [GABA]EXT) the exact origin (neuronal vs. astroglial, synaptic vs. extrasynaptic) of Glu and GABA present in dialysate samples is still a matter of debate. For better understanding the significance of in vivo microdialysis data, here we discuss methodological details and problems in addition to regulation of [Glu]EXT and [GABA]EXT. Changes in [Glu]EXT and [GABA]EXT under pathological conditions such as ischemia and epilepsy are also reviewed. Based on recent in vivo microdialysis data we argue that ambient [Glu]EXT and [GABA]EXT may have a functional role. It is suggested that specific changes in concentrations of Glu and GABA in dialysate samples together with their alterations independent of neuronal activity indicate the involvement of Glu and GABA in the information processing of the brain as essential signaling molecules of nonsynaptic transmission as well. Since various drugs are able to interfere with extrasynaptic signals in vivo, studying the extracellular cell-to-cell communication of brain cells represents a new aspect to improve drugs modulating Gluergic as well as GABAergic neurotransmission.},
	year = {2006},
	eissn = {1873-4294},
	pages = {935-940},
	orcid-numbers = {Kékesi, Adrienna Katalin/0000-0003-3042-4878; Juhász, Gábor Dénes/0000-0002-0849-6931}
}

@article{MTMT:10090417,
	title = {Taxonomic distribution and quantitative analysis of free purine and pyrimidine nucleosides in snake venoms},
	url = {https://m2.mtmt.hu/api/publication/10090417},
	author = {Aird, SD},
	doi = {10.1016/j.cbpc.2004.09.020},
	journal-iso = {COMP BIOCHEM PHYS B},
	journal = {COMPARATIVE BIOCHEMISTRY AND PHYSIOLOGY B-BIOCHEMISTRY & MOLECULAR BIOLOGY},
	volume = {140},
	unique-id = {10090417},
	issn = {1096-4959},
	year = {2005},
	eissn = {1879-1107},
	pages = {109-126}
}

@article{MTMT:109416,
	title = {Uridine release during aminopyridine-induced epilepsy},
	url = {https://m2.mtmt.hu/api/publication/109416},
	author = {Slézia, Andrea and Kékesi, Adrienna Katalin and Szikra, T and Papp, AM and Nagy, K and Szente, Magdolna and Maglóczky, Zsófia and Freund, Tamás and Juhász, Gábor Dénes},
	doi = {10.1016/j.nbd.2004.02.011},
	journal-iso = {NEUROBIOL DIS},
	journal = {NEUROBIOLOGY OF DISEASE},
	volume = {16},
	unique-id = {109416},
	issn = {0969-9961},
	year = {2004},
	eissn = {1095-953X},
	pages = {490-499},
	orcid-numbers = {Slézia, Andrea/0000-0002-4528-3169; Kékesi, Adrienna Katalin/0000-0003-3042-4878; Juhász, Gábor Dénes/0000-0002-0849-6931}
}

@article{MTMT:112734,
	title = {Characterisation of an uridine-specific binding site in rat cerebrocortical homogenates},
	url = {https://m2.mtmt.hu/api/publication/112734},
	author = {Kovács, Ilona and Lasztóczi, Bálint and Szárics, Éva and Héja, László and Sági, Gyula and Kardos, Julianna},
	doi = {10.1016/S0197-0186(03)00007-X},
	journal-iso = {NEUROCHEM INT},
	journal = {NEUROCHEMISTRY INTERNATIONAL},
	volume = {43},
	unique-id = {112734},
	issn = {0197-0186},
	year = {2003},
	eissn = {1872-9754},
	pages = {101-112}
}

@article{MTMT:33641643,
	title = {Biochemical regulation of non-rapid-eye-movement sleep},
	url = {https://m2.mtmt.hu/api/publication/33641643},
	author = {Obal, Jr. F. and Krueger, J.M.},
	doi = {10.2741/1033},
	journal-iso = {FRONT BIOSCI-LANDMARK},
	journal = {FRONTIERS IN BIOSCIENCE-LANDMARK},
	volume = {8},
	unique-id = {33641643},
	issn = {2768-6701},
	abstract = {The concept, that sleep regulatory substances (sleep factors) exist, stems from classical endocrinology and is supported by positive transfer experiments in which tissue fluids obtained from sleepy or sleeping animals elicited sleep when injected into recipient animals. The transfer experiments concluded with the identification of four sleep factors: delta sleep-inducing peptide (DSIP), uridine, oxidized glutathione, and a muramyl peptide. A physiological sleep regulatory role, however, has not been determined for these substances. In contrast, transfer experiments did not play a part in the development of the strong experimental evidence that implicated the currently known sleep factors in sleep regulation. These substances include adenosine, prostaglandin D2 (PGD2), growth hormone-releasing hormone (GHRH), interleukin-1 (IL1) and tumor necrosis factor (TNF). They promote non-REMS in various species, inhibition of their action or endogenous production results in loss of spontaneous sleep, and their synthesis and/or release display variations correlating with sleep-wake activity. Although the source of these substances vary they all enhance sleep by acting in the basal forebrain / anterior hypothalamus - preoptic region. It is also characteristic of these substances that they interact in multiple ways often resulting in mutual stimulation or potentiation of each other. Finally, there is a third group of substances whose significance in sleep regulation is less clear but for which there are two or more lines of evidence suggesting that they may have a role in modulating non-REM sleep (NREMS). This group includes oleamide, cortistatin, cholecystokinin (CCK), insulin, and nitric oxide (NO). More sleep regulatory substances are likely to be discovered in the future although it is a long and difficult process requiring multiple laboratories to generate sufficient convincing data to implicate any one of them in sleep regulation.},
	keywords = {Animals; Humans; Preoptic area; FOREBRAIN; GROWTH HORMONE; CYTOKINE PRODUCTION; tumor necrosis factor alpha; cytokine; review; review; human; animal; physiology; PROTEIN SECRETION; CHOLECYSTOKININ; HORMONES; INSULIN; nonhuman; Animalia; EEG; sleep waking cycle; nonREM sleep; Sleep, REM; sleep; REM sleep; cholinergic nerve cell; nerve ending; somatomedin C; uridine; prostaglandin D2; adenosine; protein synthesis; nitric oxide; interleukin 1beta; Glutathione Disulfide; TNF; cell activity; growth hormone releasing factor; sleep regulation; delta sleep inducing peptide; oleamide; hypothalamus; muramyl peptide},
	year = {2003},
	eissn = {2768-6698},
	pages = {d520-d550}
}