@article{MTMT:3167675,
	title = {Synaptic Reorganization of the Perisomatic Inhibitory Network in Hippocampi of Temporal Lobe Epileptic Patients},
	url = {https://m2.mtmt.hu/api/publication/3167675},
	author = {Wittner, Lucia and Maglóczky, Zsófia},
	doi = {10.1155/2017/7154295},
	journal-iso = {BIOMED RES INT},
	journal = {BIOMED RESEARCH INTERNATIONAL},
	volume = {2017},
	unique-id = {3167675},
	issn = {2314-6133},
	year = {2017},
	eissn = {2314-6141},
	orcid-numbers = {Wittner, Lucia/0000-0001-6800-0953}
}

@article{MTMT:3015678,
	title = {Intracranial neuronal ensemble recordings and analysis in epilepsy.},
	url = {https://m2.mtmt.hu/api/publication/3015678},
	author = {Tóth, Emília and Fabó, Dániel and Entz, László and Ulbert, István and Erőss, Loránd},
	doi = {10.1016/j.jneumeth.2015.09.028},
	journal-iso = {J NEUROSCI METH},
	journal = {JOURNAL OF NEUROSCIENCE METHODS},
	volume = {260},
	unique-id = {3015678},
	issn = {0165-0270},
	abstract = {Pathological neuronal firing was demonstrated 50 years ago as the hallmark of epileptically transformed cortex with the use of implanted microelectrodes. Since then, microelectrodes remained only experimental tools in humans to detect unitary neuronal activity to reveal physiological and pathological brain functions. This recording technique has evolved substantially in the past few decades; however, based on recent human data implying their usefulness as diagnostic tools, we expect a substantial increase in the development of microelectrodes in the near future. Here, we review the technological background and history of microelectrode array development for human examinations in epilepsy, including discussions on of wire-based and microelectrode arrays fabricated using micro-electro-mechanical system (MEMS) techniques and novel future techniques to record neuronal ensemble. We give an overview of clinical and surgical considerations, and try to provide a list of probes on the market with their availability for human recording. Then finally, we briefly review the literature on modulation of single neuron for the treatment of epilepsy, and highlight the current topics under examination that can be background for the future development.},
	year = {2016},
	eissn = {1872-678X},
	pages = {261-269},
	orcid-numbers = {Fabó, Dániel/0000-0001-5141-5351; Ulbert, István/0000-0001-9941-9159; Erőss, Loránd/0000-0002-5796-5546}
}

@article{MTMT:1774591,
	title = {Redistribution of CB1 Cannabinoid Receptors in the Acute and Chronic Phases of Pilocarpine-Induced Epilepsy},
	url = {https://m2.mtmt.hu/api/publication/1774591},
	author = {Karlócai, Rita and Tóth, Kinga and Watanabe, M and Ledent, C and Juhász, Gábor Dénes and Freund, Tamás and Maglóczky, Zsófia},
	doi = {10.1371/journal.pone.0027196},
	journal-iso = {PLOS ONE},
	journal = {PLOS ONE},
	volume = {6},
	unique-id = {1774591},
	issn = {1932-6203},
	abstract = {The endocannabinoid system plays a central role in retrograde synaptic communication and may control the spread of activity in an epileptic network. Using the pilocarpine model of temporal lobe epilepsy we examined the expression pattern of the Type 1 cannabinoid receptor (CB1-R) in the hippocampi of CD1 mice at survival times of 2 hours, 1 day, 3 days and 2 months (acute, latent and chronic phases). Based on the behavioral signs of the acute seizures, animals were classified as "weakly" or "strongly" epileptic using the modified Racine scale. Mice of the weak group had mild seizures, whereas seizures in the strong group were frequent with intense motor symptoms and the majority of these animals developed sclerosis in the chronic phase. In control samples the most intense staining of CB1-R-positive fibers was found in the molecular layer of the dentate gyrus and in str. pyramidale of the cornu Ammonis. In weak animals no significant changes were seen at any survival time compared to controls. In strong animals, however, in the acute phase, a massive reduction in CB1-R-stained terminals occurred in the hippocampus. In the latent phase CB1-R immunoreactivity gradually recovered. In the chronic phase, CB1-immunostaining in sclerotic samples was stronger throughout the hippocampus. Quantitative electron microscopic analysis showed an increase in the number of CB1-R-positive terminals in the dentate gyrus. Moreover, the number of immunogold particles significantly increased in GABAergic terminals. Our results suggest a proconvulsive downregulation of CB1 receptors in the acute phase most probably due to receptor internalization, followed by compensatory upregulation and sprouting in the chronic phase of epilepsy. In conclusion, the changes in CB1 receptor expression pattern revealed in this study are associated with the severity of hippocampal injury initiated by acute seizures that ultimately leads to sclerosis in the vulnerable regions in the chronic phase.},
	year = {2011},
	eissn = {1932-6203},
	pages = {27196},
	orcid-numbers = {Tóth, Kinga/0000-0002-8751-8499; Juhász, Gábor Dénes/0000-0002-0849-6931}
}

@article{MTMT:109357,
	title = {Synaptic reorganization of calbindin-positive neurons in the human hippocampal CA1 region in temporal lobe epilepsy},
	url = {https://m2.mtmt.hu/api/publication/109357},
	author = {Wittner, Lucia and Erőss, Loránd and Szabó, Z and Tóth, Sz and Czirják, Sándor and Halász, Péter and Freund, Tamás and Maglóczky, Zsófia},
	doi = {10.1016/S0306-4522(02)00264-6},
	journal-iso = {NEUROSCIENCE},
	journal = {NEUROSCIENCE},
	volume = {115},
	unique-id = {109357},
	issn = {0306-4522},
	abstract = {The distribution, morphology, synaptic coverage and postsynaptic targets of calbindin-containing interneurons and afferent pathways have been analyzed in the control and epileptic CA1 region of the human hippocampus. Numerous calbindin-positive interneurons are preserved even in the strongly sclerotic CA1 region. The morphology of individual cells is altered: the cell body and dendrites become spiny, the radially oriented dendrites disappear, and are replaced by a large number of curved, distorted dendrites. Even in the non-sclerotic epileptic samples, where pyramidal cells are present and calbindin-immunoreactive interneurons seem to be unchanged, some modifications could be observed at the electron microscopic level: they received more inhibitory synaptic input, and the calbindin-positive excitatory afferents - presumably derived from the CA1, the CA2 and/or the dentate gyrus - are sprouted. In the strongly sclerotic tissue, with the death of pyramidal cells, calbindin-positive terminals (belonging to interneurons and the remaining excitatory afferents) change their targets. Our data suggest that an intense synaptic reorganization takes place in the epileptic CA1 region, even in the non-sclerotic tissue, before the death of considerable numbers of pyramidal cells. Calbindin-positive interneurons participate in this reorganization: they show plastic changes in response to epilepsy. The enhanced inhibition of inhibitory interneurons may result in the disinhibition of pyramidal cells or in an abnormal synchrony in the output region of the hippocampus. © 2002 IBRO. Published by Elsevier Science Ltd. All rights reserved.},
	keywords = {Adult; Adult; Female; Female; Middle Aged; Male; Male; Humans; immunohistochemistry; hippocampus; hippocampus; ARTICLE; human; Microscopy, Electron; MORPHOLOGY; priority journal; controlled study; Epilepsy, Temporal Lobe; brain region; SYNAPSES; PLASTICITY; PYRAMIDAL CELLS; nerve cell; Presynaptic Terminals; human cell; SCLEROSIS; calbindin; sensory nerve; Afferent Pathways; Cell Death; pyramidal nerve cell; interneuron; Temporal lobe epilepsy; Neuronal Plasticity; Dendrites; Calcium-Binding Protein, Vitamin D-Dependent; Synaptic Membranes; axonal sprouting; Chandelier cell; Inhibitory input; Network reorganization; interneurons},
	year = {2002},
	eissn = {1873-7544},
	pages = {961-978},
	orcid-numbers = {Wittner, Lucia/0000-0001-6800-0953; Erőss, Loránd/0000-0002-5796-5546; Czirják, Sándor/0000-0002-8224-3561}
}