@article{MTMT:34768350,
	title = {Simulation of gap junction formation reveals critical role of Cys disulfide redox state in connexin hemichannel docking},
	url = {https://m2.mtmt.hu/api/publication/34768350},
	author = {Héja, László and Simon, Ágnes and Kardos, Julianna},
	doi = {10.1186/s12964-023-01439-z},
	journal-iso = {CELL COMM SIGN},
	journal = {CELL COMMUNICATION AND SIGNALING},
	volume = {22},
	unique-id = {34768350},
	issn = {1478-811X},
	year = {2024},
	eissn = {1478-811X}
}

@article{MTMT:34718118,
	title = {GABA fluctuations driven by astrocytic Glu-GABA exchange explain synaptic acuity},
	url = {https://m2.mtmt.hu/api/publication/34718118},
	author = {Héja, László and Kardos, Julianna},
	doi = {10.46439/signaling.1.016},
	journal-iso = {Cell Signal},
	journal = {Cell Signaling},
	volume = {1},
	unique-id = {34718118},
	year = {2023},
	eissn = {2837-8253},
	pages = {76-80}
}

@article{MTMT:32612048,
	title = {Connexons coupling to gap junction channel: Potential role for extracellular protein stabilization centers},
	url = {https://m2.mtmt.hu/api/publication/32612048},
	author = {Héja, László and Simon, Ágnes and Szabó, Zsolt and Kardos, Julianna},
	doi = {10.3390/biom12010049},
	journal-iso = {BIOMOLECULES},
	journal = {BIOMOLECULES},
	volume = {12},
	unique-id = {32612048},
	issn = {2218-273X},
	abstract = {Connexin (Cx) proteins establish intercellular gap junction channels (Cx GJCs) through coupling of two apposed hexameric Cx hemichannels (Cx HCs, connexons). Pre-and post-GJ interfaces consist of extracellular EL1 and EL2 loops, each with three conserved cysteines. Previously, we reported that known peptide inhibitors, mimicking a variety of Cx43 sequences, appear non-selective when binding to homomeric Cx43 vs. Cx36 GJC homology model subtypes. In pursuit of finding potentially Cx subtype-specific inhibitors of connexon-connexon coupling, we aimed at to understand better how the GJ interface is formed. Here we report on the discovery of Cx GJC subtype-specific protein stabilization centers (SCs) featuring GJ interface architecture. First, the Cx43 GJC homology model, embedded in two opposed membrane bilayers, has been devised. Next, we endorsed the fluctuation dynamics of SCs of the interface domain of Cx43 GJC by applying standard molecular dynamics under open and closed cystine disulfide bond (CS-SC) preconditions. The simulations confirmed the major role of of the unique trans-GJ SC pattern comprising conserved (55N, 56T) and non-conserved (57Q) residues of the apposed EL1 loops in the stabilization of the GJC complex. Importantly, clusters of SC patterns residing close to the GJ interface domain appear to orient the interface formation via the numerous SCs between EL1 and EL2. These include central54CS-S198C or61CS-S192C contacts with residues 53R, 54C, 55N, 197D, 199F or 64V, 191P, respectively. In addition, we revealed that GJC interface formation is favoured when the psi dihedral angle of the nearby 193P residue is stable around 180◦ and the interface SCs disappear when this angle moves to the 0◦ to −45◦ range. The potential of the association of non-conserved residues with SC motifs in connexon-connexon coupling makes the development of Cx subtype-specific inhibitors viable. © 2021 by the authors. Licensee MDPI, Basel, Switzerland.},
	keywords = {ARTICLE; human; membrane protein; nonhuman; PROTEIN FUNCTION; molecular dynamics; computer model; gap junction protein; disulfide bond; Connexin 43; Cystine; bilayer membrane; connexon; Close/open disulfide bonds precon-ditions; Cx43 GJC with two membranes; Cystine disulfide related GJ SC patterns; Fluctuation dynamics of protein stabilization centres (SCs); GJ architecture; Subtype-specific SC motifs},
	year = {2022},
	eissn = {2218-273X},
	orcid-numbers = {Szabó, Zsolt/0000-0002-2902-743X}
}

@article{MTMT:33031938,
	title = {Putrescine Intensifies Glu/GABA Exchange Mechanism and Promotes Early Termination of Seizures},
	url = {https://m2.mtmt.hu/api/publication/33031938},
	author = {Kovács, Zsolt and Skatchkov, Serguei N. and Szabó, Zsolt and Qahtan, Saif and Méndez-González, Miguel P. and Malpica-Nieves, Christian J. and Eaton, Misty J. and Kardos, Julianna and Héja, László},
	doi = {10.3390/ijms23158191},
	journal-iso = {INT J MOL SCI},
	journal = {INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES},
	volume = {23},
	unique-id = {33031938},
	issn = {1661-6596},
	year = {2022},
	eissn = {1422-0067},
	orcid-numbers = {Kovács, Zsolt/0000-0001-8571-5686; Szabó, Zsolt/0000-0002-2902-743X; Méndez-González, Miguel P./0000-0003-0079-4042; Malpica-Nieves, Christian J./0000-0001-6778-408X}
}

@article{MTMT:32578354,
	title = {Critical Role of Astrocytic Polyamine and GABA Metabolism in Epileptogenesis},
	url = {https://m2.mtmt.hu/api/publication/32578354},
	author = {Kovács, Zsolt and Skatchkov, Serguei N. and Veh, Rüdiger W. and Szabó, Zsolt and Németh, Krisztina and Szabó, Pál Tamás and Kardos, Julianna and Héja, László},
	doi = {10.3389/fncel.2021.787319},
	journal-iso = {FRONT CELL NEUROSCI},
	journal = {FRONTIERS IN CELLULAR NEUROSCIENCE},
	volume = {15},
	unique-id = {32578354},
	issn = {1662-5102},
	year = {2022},
	eissn = {1662-5102},
	orcid-numbers = {Kovács, Zsolt/0000-0001-8571-5686; Szabó, Zsolt/0000-0002-2902-743X; Szabó, Pál Tamás/0000-0003-2260-4641}
}

@article{MTMT:31925857,
	title = {Spontaneous Ca2+ Fluctuations Arise in Thin Astrocytic Processes With Real 3D Geometry},
	url = {https://m2.mtmt.hu/api/publication/31925857},
	author = {Héja, László and Szabó, Zsolt and Péter, Márton and Kardos, Julianna},
	doi = {10.3389/fncel.2021.617989},
	journal-iso = {FRONT CELL NEUROSCI},
	journal = {FRONTIERS IN CELLULAR NEUROSCIENCE},
	volume = {15},
	unique-id = {31925857},
	issn = {1662-5102},
	year = {2021},
	eissn = {1662-5102},
	orcid-numbers = {Szabó, Zsolt/0000-0002-2902-743X}
}

@article{MTMT:31971626,
	title = {Dual Role for Astroglial Copper-Assisted Polyamine Metabolism during Intense Network Activity},
	url = {https://m2.mtmt.hu/api/publication/31971626},
	author = {Szabó, Zsolt and Péter, Márton and Héja, László and Kardos, Julianna},
	doi = {10.3390/biom11040604},
	journal-iso = {BIOMOLECULES},
	journal = {BIOMOLECULES},
	volume = {11},
	unique-id = {31971626},
	issn = {2218-273X},
	year = {2021},
	eissn = {2218-273X},
	orcid-numbers = {Szabó, Zsolt/0000-0002-2902-743X; Kardos, Julianna/0000-0001-9873-7155}
}

@article{MTMT:31123982,
	title = {NCX activity generates spontaneous Ca2+ oscillations in the astrocytic leaflet microdomain},
	url = {https://m2.mtmt.hu/api/publication/31123982},
	author = {Héja, László and Kardos, Julianna},
	doi = {10.1016/j.ceca.2019.102137},
	journal-iso = {CELL CALCIUM},
	journal = {CELL CALCIUM},
	volume = {86},
	unique-id = {31123982},
	issn = {0143-4160},
	abstract = {The synergy between synaptic Glu release and astrocytic Glu-Na+ symport is essential to the signalling function of the tripartite synapse. Here we used kinetic data of astrocytic Glu transporters (EAAT) and the Na+/Ca2+ exchanger (NCX) to simulate Glu release, Glu uptake and subsequent Na+ and Ca2+ dynamics in the astrocytic leaflet microdomain following single release event. Model simulations show that Glu-Na+ symport differently affect intracellular [Na+] in synapses with different extent of astrocytic coverage. Surprisingly, NCX activity alone has been shown to generate markedly stable, spontaneous Ca2+ oscillation in the astrocytic leaflet. These on-going oscillations appear when NCX operates either in the forward or reverse direction. We conjecture that intrinsic NCX activity may play a prominent role in the generation of astrocytic Ca2+ oscillations. © 2019 The Authors},
	keywords = {ARTICLE; priority journal; nonhuman; brain region; Sodium ion; Calcium ion; nerve cell; glutamic acid; amino acid transport; molecular dynamics; Calcium Signaling; ASTROCYTE; anion exchange; intracellular transport; Na+/Ca2+ exchange; CA2+ OSCILLATIONS; membrane microdomain; Astrocytic Glu-Na+ symport; Astrocytic leaflet; Glu-Na+ symport; Synaptic Glu release; membrane leaflet},
	year = {2020},
	eissn = {1532-1991}
}

@article{MTMT:31795296,
	title = {Peptide Binding Sites of Connexin Proteins},
	url = {https://m2.mtmt.hu/api/publication/31795296},
	author = {Simon, Ágnes and Magyar, Csaba and Héja, László and Kardos, Julianna},
	doi = {10.3390/chemistry2030042},
	journal-iso = {CHEMISTRY},
	journal = {CHEMISTRY},
	volume = {2},
	unique-id = {31795296},
	year = {2020},
	eissn = {2624-8549},
	pages = {662-673},
	orcid-numbers = {Magyar, Csaba/0000-0002-5023-6180}
}

@article{MTMT:30721430,
	title = {Feedback adaptation of synaptic excitability via Glu:Na+ symport driven astrocytic GABA and Gln release},
	url = {https://m2.mtmt.hu/api/publication/30721430},
	author = {Héja, László and Simon, Ágnes and Szabó, Zsolt and Kardos, Julianna},
	doi = {10.1016/j.neuropharm.2019.05.006},
	journal-iso = {NEUROPHARMACOLOGY},
	journal = {NEUROPHARMACOLOGY},
	volume = {161},
	unique-id = {30721430},
	issn = {0028-3908},
	year = {2019},
	eissn = {1873-7064},
	orcid-numbers = {Szabó, Zsolt/0000-0002-2902-743X}
}

@article{MTMT:30694084,
	title = {Molecular Plasticity of the Nucleus Accumbens Revisited—Astrocytic Waves Shall Rise},
	url = {https://m2.mtmt.hu/api/publication/30694084},
	author = {Kardos, Julianna and Dobolyi, Árpád and Szabó, Zsolt and Simon, Ágnes and Lourmet, Guillaume and Palkovits, Miklós and Héja, László},
	doi = {10.1007/s12035-019-1641-z},
	journal-iso = {MOL NEUROBIOL},
	journal = {MOLECULAR NEUROBIOLOGY},
	volume = {56},
	unique-id = {30694084},
	issn = {0893-7648},
	year = {2019},
	eissn = {1559-1182},
	pages = {7950-7965},
	orcid-numbers = {Dobolyi, Árpád/0000-0003-0397-2991; Szabó, Zsolt/0000-0002-2902-743X; Palkovits, Miklós/0000-0003-0578-0387}
}

@article{MTMT:31096625,
	title = {Astrocytic gap junctions differentially affect seizures in absence and temporal lobe epilepsy models},
	url = {https://m2.mtmt.hu/api/publication/31096625},
	author = {Vincze, R. and Péter, Márton and Szabó, Zsolt and Kardos, Julianna and Kovács, Zsolt and Héja, László},
	journal-iso = {GLIA},
	journal = {GLIA},
	volume = {67},
	unique-id = {31096625},
	issn = {0894-1491},
	year = {2019},
	eissn = {1098-1136},
	pages = {E710-E711},
	orcid-numbers = {Szabó, Zsolt/0000-0002-2902-743X; Kovács, Zsolt/0000-0001-8571-5686}
}

@article{MTMT:30685187,
	title = {Connexin 43 Differentially Regulates Epileptiform Activity in Models of Convulsive and Non-Convulsive Epilepsies},
	url = {https://m2.mtmt.hu/api/publication/30685187},
	author = {Vincze, Renáta and Péter, Márton and Szabó, Zsolt and Kardos, Julianna and Héja, László and Kovács, Zsolt},
	doi = {10.3389/fncel.2019.00173},
	journal-iso = {FRONT CELL NEUROSCI},
	journal = {FRONTIERS IN CELLULAR NEUROSCIENCE},
	volume = {13},
	unique-id = {30685187},
	issn = {1662-5102},
	year = {2019},
	eissn = {1662-5102},
	orcid-numbers = {Szabó, Zsolt/0000-0002-2902-743X; Kovács, Zsolt/0000-0001-8571-5686}
}

@article{MTMT:30379283,
	title = {Copper signalling: causes and consequences (vol 16, 71 , 2018)},
	url = {https://m2.mtmt.hu/api/publication/30379283},
	author = {Kardos, Julianna and Héja, László and Simon, Ágnes and Jablonkai, István and Kovacs, Richard and Jemnitz, Katalin},
	doi = {10.1186/s12964-018-0292-4},
	journal-iso = {CELL COMM SIGN},
	journal = {CELL COMMUNICATION AND SIGNALING},
	volume = {16},
	unique-id = {30379283},
	issn = {1478-811X},
	abstract = {Following publication of the original article [1], the authors reported an error in Table 3. The correct version of Table 3 is shown below:The publishers apologise for this error. The original article [1] has been corrected.},
	year = {2018},
	eissn = {1478-811X}
}

@article{MTMT:30317831,
	title = {Copper signalling: causes and consequences},
	url = {https://m2.mtmt.hu/api/publication/30317831},
	author = {Kardos, Julianna and Héja, László and Simon, Ágnes and Jablonkai, István and Kovács, Richárd and Jemnitz, Katalin},
	doi = {10.1186/s12964-018-0277-3},
	journal-iso = {CELL COMM SIGN},
	journal = {CELL COMMUNICATION AND SIGNALING},
	volume = {16},
	unique-id = {30317831},
	issn = {1478-811X},
	abstract = {Copper-containing enzymes perform fundamental functions by activating dioxygen (O-2) and therefore allowing chemical energy-transfer for aerobic metabolism. The copper-dependence of O-2 transport, metabolism and production of signalling molecules are supported by molecular systems that regulate and preserve tightly-bound static and weakly-bound dynamic cellular copper pools. Disruption of the reducing intracellular environment, characterized by glutathione shortage and ambient Cu(II) abundance drives oxidative stress and interferes with the bidirectional, copper-dependent communication between neurons and astrocytes, eventually leading to various brain disease forms. A deeper understanding of of the regulatory effects of copper on neuro-glia coupling via polyamine metabolism may reveal novel copper signalling functions and new directions for therapeutic intervention in brain disorders associated with aberrant copper metabolism.},
	keywords = {GSH; Redox disproportionation and speciation of copper; Dynamic copper pool; Copper-rich aggregates; GSSG ratio; Copper chelate therapy; Neuro-glia coupling},
	year = {2018},
	eissn = {1478-811X}
}

@article{MTMT:3209058,
	title = {The nature of early astroglial protection-Fast activation and signaling.. Fast activation and signaling},
	url = {https://m2.mtmt.hu/api/publication/3209058},
	author = {Kardos, Julianna and Héja, László and Jemnitz, Katalin and Kovacs, R and Palkovits, Miklós},
	doi = {10.1016/j.pneurobio.2017.03.005},
	journal-iso = {PROG NEUROBIOL},
	journal = {PROGRESS IN NEUROBIOLOGY: AN INTERNATIONAL REVIEW JOURNAL},
	volume = {153},
	unique-id = {3209058},
	issn = {0301-0082},
	abstract = {Our present review is focusing on the uniqueness of balanced 
		astroglial signaling. The balance of excitatory and inhibitory 
		signaling within the CNS is mainly determined by sharp synaptic 
		transients of excitatory glutamate (Glu) and inhibitory gamma-
		aminobutyrate (GABA) acting on the sub-second timescale. 
		Astroglia is involved in excitatory chemical transmission by 
		taking up i) Glu through neurotransmitter-sodium transporters, 
		ii) K+ released due to presynaptic action potential generation, 
		and iii) water keeping osmotic pressure. Glu uptake-coupled Na+ 
		influx may either ignite long-range astroglial Ca2+ transients 
		or locally counteract over-excitation via astroglial GABA 
		release and increased tonic inhibition. Imbalance of excitatory 
		and inhibitory drives is associated with a number of disease 
		conditions, including prevalent traumatic and ischaemic 
		injuries or the emergence of epilepsy. Therefore, when 
		addressing the potential of early therapeutic intervention, 
		astroglial signaling functions combating progress of Glu 
		excitotoxicity is of critical importance. We suggest, that 
		excitotoxicity is linked primarily to over-excitation induced by 
		the impairment of astroglial Glu uptake and/or GABA release. 
		Within this framework, we discuss the acute alterations of Glu-
		cycling and metabolism and conjecture the therapeutic promise of 
		regulation. We also confer the role played by key carrier 
		proteins and enzymes as well as their interplay at the 
		molecular, cellular, and organ levels. Moreover, based on our 
		former studies, we offer potential prospect on the emerging 
		theme of astroglial succinate sensing in course of Glu 
		excitotoxicity.},
	year = {2017},
	eissn = {1873-5118},
	pages = {86-99},
	orcid-numbers = {Palkovits, Miklós/0000-0003-0578-0387}
}

@article{MTMT:3251043,
	title = {Extensive astrocyte synchronization advances neuronal coupling in slow wave activity in vivo},
	url = {https://m2.mtmt.hu/api/publication/3251043},
	author = {Szabó, Zsolt and Héja, László and Szalay, Gergely and Kékesi, Orsolya Sára and Füredi, András and Szebényi, Kornélia and Dobolyi, Árpád and Orbán, Tamás I. and Kolacsek, Orsolya and Tompa, Tamás and Miskolczy, Zsombor and Biczók, László and Rózsa J., Balázs and Sarkadi, Balázs and Kardos, Julianna},
	doi = {10.1038/s41598-017-06073-7},
	journal-iso = {SCI REP},
	journal = {SCIENTIFIC REPORTS},
	volume = {7},
	unique-id = {3251043},
	issn = {2045-2322},
	abstract = {Slow wave activity (SWA) is a characteristic brain oscillation in sleep and quiet wakefulness. Although the cell types contributing to SWA genesis are not yet identified, the principal role of neurons in the emergence of this essential cognitive mechanism has not been questioned. To address the possibility of astrocytic involvement in SWA, we used a transgenic rat line expressing a calcium sensitive fluorescent protein in both astrocytes and interneurons and simultaneously imaged astrocytic and neuronal activity in vivo. Here we demonstrate, for the first time, that the astrocyte network display synchronized recurrent activity in vivo coupled to UP states measured by field recording and neuronal calcium imaging. Furthermore, we present evidence that extensive synchronization of the astrocytic network precedes the spatial build-up of neuronal synchronization. The earlier extensive recruitment of astrocytes in the synchronized activity is reinforced by the observation that neurons surrounded by active astrocytes are more likely to join SWA, suggesting causality. Further supporting this notion, we demonstrate that blockade of astrocytic gap junctional communication or inhibition of astrocytic Ca2+ transients reduces the ratio of both astrocytes and neurons involved in SWA. These in vivo findings conclusively suggest a causal role of the astrocytic syncytium in SWA generation.},
	keywords = {HUMAN BRAIN; CEREBRAL-CORTEX; sleep; tonic inhibition; NETWORK MECHANISMS; LESS-THAN-1 HZ; GABA RELEASE; Calcium dynamics; GAP-JUNCTION; interneurons},
	year = {2017},
	eissn = {2045-2322},
	orcid-numbers = {Szabó, Zsolt/0000-0002-2902-743X; Füredi, András/0000-0002-7883-9901; Szebényi, Kornélia/0000-0003-1558-8372; Dobolyi, Árpád/0000-0003-0397-2991; Orbán, Tamás I./0000-0002-3424-3428; Biczók, László/0000-0003-2568-5942; Sarkadi, Balázs/0000-0003-0592-4539}
}

@article{MTMT:2972586,
	title = {Framing Neuro-Glia Coupling in Antiepileptic Drug Design.},
	url = {https://m2.mtmt.hu/api/publication/2972586},
	author = {Kardos, Julianna and Szabó, Zsolt and Héja, László},
	doi = {10.1021/acs.jmedchem.5b00331},
	journal-iso = {J MED CHEM},
	journal = {JOURNAL OF MEDICINAL CHEMISTRY},
	volume = {59},
	unique-id = {2972586},
	issn = {0022-2623},
	abstract = {We delineate perspectives for the design and discovery of antiepileptic drugs (AEDs) with fewer side effects by focusing on astroglial modulation of spatiotemporal seizure dynamics. It is now recognized that the major inhibitory neurotransmitter of the brain, gamma-aminobutyric acid (GABA), can be released through the reversal of astroglial GABA transporters. Synaptic spillover and subsequent glutamate (Glu) uptake in neighboring astrocytes evoke replacement of extracellular Glu for GABA, driving neurons away from the seizure threshold. Attenuation of synaptic signaling by this negative feedback through the interplay of Glu and GABA transporters of adjacent astroglia can result in shortened seizures. By contrast, long-range activation of astroglia through gap junctions may promote recurrent seizures on the model of pharmacoresistant temporal lobe epilepsy. From their first detection to our current understanding, we identify various targets that shape both short- and long-range neuro-astroglia coupling, as these are manifest in epilepsy phenomena and in the associated research promotions of AED.},
	year = {2016},
	eissn = {1520-4804},
	pages = {777-787},
	orcid-numbers = {Szabó, Zsolt/0000-0002-2902-743X}
}

@article{MTMT:2972585,
	title = {Astrocyte sodium signaling and the regulation of neurotransmission},
	url = {https://m2.mtmt.hu/api/publication/2972585},
	author = {Kirischuk, S and Héja, László and Kardos, Julianna and Billups, B},
	doi = {10.1002/glia.22943},
	journal-iso = {GLIA},
	journal = {GLIA},
	volume = {64},
	unique-id = {2972585},
	issn = {0894-1491},
	abstract = {The transmembrane Na+ concentration gradient is an important source of energy required not only to enable the generation of action potentials in excitable cells, but also for various transmembrane transporters both in excitable and non-excitable cells, like astrocytes. One of the vital functions of astrocytes in the central nervous system (CNS) is to regulate neurotransmitter concentrations in the extracellular space. Most neurotransmitters in the CNS are removed from the extracellular space by Na+ -dependent neurotransmitter transporters (NeuTs) expressed both in neurons and astrocytes. Neuronal NeuTs control mainly phasic synaptic transmission, i.e., synaptically induced transient postsynaptic potentials, while astrocytic NeuTs contribute to the termination of phasic neurotransmission and modulate the tonic tone, i.e., the long-lasting activation of extrasynaptic receptors by neurotransmitter that has diffused out of the synaptic cleft. Consequently, local intracellular Na+ ([Na+ ]i ) transients occurring in astrocytes, for example via the activation of ionotropic neurotransmitter receptors, can affect the driving force for neurotransmitter uptake, in turn modulating the spatio-temporal profiles of neurotransmitter levels in the extracellular space. As some NeuTs are close to thermodynamic equilibrium under resting conditions, an increase in astrocytic [Na+ ]i can stimulate the direct release of neurotransmitter via NeuT reversal. In this review we discuss the role of astrocytic [Na+ ]i changes in the regulation of uptake/release of neurotransmitters. It is emphasized that an activation of one neurotransmitter system, including either its ionotropic receptor or Na+ -coupled co-transporter, can strongly influence, or even reverse, other Na+ -dependent NeuTs, with potentially significant consequences for neuronal communication. GLIA 2015.},
	year = {2016},
	eissn = {1098-1136},
	pages = {1655-1666}
}

@article{MTMT:2988827,
	title = {Straightforward and effective synthesis of gamma-aminobutyric acid transporter subtype 2-selective acyl-substituted azaspiro[4.5]decanes},
	url = {https://m2.mtmt.hu/api/publication/2988827},
	author = {Ma, X and Lubin, H and Ioja, Enikő and Kékesi, Orsolya Sára and Simon, Ágnes and Apáti, Ágota and Orbán, Tamás I. and Héja, László and Kardos, Julianna and Marko, IE},
	doi = {10.1016/j.bmcl.2015.11.100},
	journal-iso = {BIOORG MED CHEM LETT},
	journal = {BIOORGANIC & MEDICINAL CHEMISTRY LETTERS},
	volume = {26},
	unique-id = {2988827},
	issn = {0960-894X},
	abstract = {Supply of major metabolites such as gamma-aminobutyric acid (GABA), beta-alanine and taurine is an essential instrument that shapes signalling, proper cell functioning and survival in the brain and peripheral organs. This background motivates the synthesis of novel classes of compounds regulating their selective transport through various fluid-organ barriers via the low-affinity gamma-aminobutyric acid (GABA) transporter subtype 2 (GAT2). Natural and synthetic spirocyclic compounds or therapeutics with a range of structures and biological activity are increasingly recognised in this regard. Based on pre-validated GABA transport activity, straightforward and efficient synthesis method was developed to provide an azaspiro[4.5]decane scaffold, holding a variety of charge, substituent and 3D constrain of spirocyclic amine. Investigation of the azaspiro[4.5]decane scaffold in cell lines expressing the four GABA transporter subtypes led to the discovery of a subclass of a GAT2-selective compounds with acyl-substituted azaspiro[4.5]decane core.},
	year = {2016},
	eissn = {1464-3405},
	pages = {417-423},
	orcid-numbers = {Orbán, Tamás I./0000-0002-3424-3428}
}