@article{MTMT:34749015,
	title = {Synaptic and dendritic architecture of different types of hippocampal somatostatin interneurons},
	url = {https://m2.mtmt.hu/api/publication/34749015},
	author = {Tresóné Takács, Virág and Bardóczi, Zsuzsanna and Orosz, Áron and Major, Ábel and Tar, Luca and Berki, Péter and Papp, Péter and Mayer, Márton István and Sebők, Hunor and Zsolt, Luca and Sós, Katalin Eszter and Káli, Szabolcs and Freund, Tamás and Nyíri, Gábor},
	doi = {10.1371/journal.pbio.3002539},
	journal-iso = {PLOS BIOL},
	journal = {PLOS BIOLOGY},
	volume = {22},
	unique-id = {34749015},
	issn = {1544-9173},
	abstract = {GABAergic inhibitory neurons fundamentally shape the activity and plasticity of cortical circuits. A major subset of these neurons contains somatostatin (SOM); these cells play crucial roles in neuroplasticity, learning, and memory in many brain areas including the hippocampus, and are implicated in several neuropsychiatric diseases and neurodegenerative disorders. Two main types of SOM-containing cells in area CA1 of the hippocampus are oriens-lacunosum-moleculare (OLM) cells and hippocampo-septal (HS) cells. These cell types show many similarities in their soma-dendritic architecture, but they have different axonal targets, display different activity patterns in vivo, and are thought to have distinct network functions. However, a complete understanding of the functional roles of these interneurons requires a precise description of their intrinsic computational properties and their synaptic interactions. In the current study we generated, analyzed, and make available several key data sets that enable a quantitative comparison of various anatomical and physiological properties of OLM and HS cells in mouse. The data set includes detailed scanning electron microscopy (SEM)-based 3D reconstructions of OLM and HS cells along with their excitatory and inhibitory synaptic inputs. Combining this core data set with other anatomical data, patch-clamp electrophysiology, and compartmental modeling, we examined the precise morphological structure, inputs, outputs, and basic physiological properties of these cells. Our results highlight key differences between OLM and HS cells, particularly regarding the density and distribution of their synaptic inputs and mitochondria. For example, we estimated that an OLM cell receives about 8,400, whereas an HS cell about 15,600 synaptic inputs, about 16% of which are GABAergic. Our data and models provide insight into the possible basis of the different functionality of OLM and HS cell types and supply essential information for more detailed functional models of these neurons and the hippocampal network.},
	year = {2024},
	eissn = {1545-7885},
	orcid-numbers = {Tresóné Takács, Virág/0000-0002-3276-4131}
}

@misc{MTMT:34096335,
	title = {Parvalbumin-expressing basal forebrain neurons mediate learning from negative experience},
	url = {https://m2.mtmt.hu/api/publication/34096335},
	author = {Hegedüs, Panna and Victoria, Lyakhova and Velencei, Anna and Mayer, Márton István and Zelenak, Zsofia and Nyíri, Gábor and Hangya, Balázs},
	unique-id = {34096335},
	year = {2023},
	orcid-numbers = {Hegedüs, Panna/0000-0002-9984-5729}
}

@article{MTMT:33833304,
	title = {Fear memory recall involves hippocampal somatostatin interneurons},
	url = {https://m2.mtmt.hu/api/publication/33833304},
	author = {Zichó, Krisztián and Sós, Katalin Eszter and Papp, Péter and Barth, Albert and Misák, Erik and Orosz, Áron and Mayer, Márton István and Sebestény, Réka Z. and Nyíri, Gábor},
	doi = {10.1371/journal.pbio.3002154},
	journal-iso = {PLOS BIOL},
	journal = {PLOS BIOLOGY},
	volume = {21},
	unique-id = {33833304},
	issn = {1544-9173},
	year = {2023},
	eissn = {1545-7885}
}

@article{MTMT:33190635,
	title = {Vascular supply of the metacarpophalangeal joint},
	url = {https://m2.mtmt.hu/api/publication/33190635},
	author = {Baksa, Gábor and Czeibert, Kálmán and Sharp, Veronika and Handschuh, Stephan and Gyebnár, János and Bárány, László and Benis, Szabolcs and Nyíri, Gábor and Mandl, Peter and Petneházy, Örs and Bálint, Péter Vince},
	doi = {10.3389/fmed.2022.1015895},
	journal-iso = {FRONT MED},
	journal = {FRONTIERS IN MEDICINE},
	volume = {9},
	unique-id = {33190635},
	year = {2022},
	eissn = {2296-858X},
	orcid-numbers = {Czeibert, Kálmán/0000-0001-9425-0892; Petneházy, Örs/0000-0001-9698-5753}
}

@article{MTMT:31337319,
	title = {Amyloid β induces interneuron-specific changes in the hippocampus of APPNL-F mice},
	url = {https://m2.mtmt.hu/api/publication/31337319},
	author = {Sós, Katalin Eszter and Mayer, Márton István and Tresóné Takács, Virág and Major, Ábel and Bardóczi, Zsuzsanna and Beres, Barnabas M. and Szeles, Tamás and Saito, Takashi and Saido, Takaomi C. and Mody, István and Freund, Tamás and Nyíri, Gábor},
	doi = {10.1371/journal.pone.0233700},
	journal-iso = {PLOS ONE},
	journal = {PLOS ONE},
	volume = {15},
	unique-id = {31337319},
	issn = {1932-6203},
	year = {2020},
	eissn = {1932-6203},
	orcid-numbers = {Tresóné Takács, Virág/0000-0002-3276-4131}
}

@article{MTMT:30881269,
	title = {Median raphe controls acquisition of negative experience in the mouse},
	url = {https://m2.mtmt.hu/api/publication/30881269},
	author = {Szőnyi, András and Zichó, Krisztián and Barth, Albert and Gönczi, Roland T. and Schlingloff, Dániel and Török, Bibiána and Bodóné Sipos, Eszter and Major, Ábel and Bardóczi, Zsuzsanna and Sós, Katalin Eszter and Gulyás, Attila and Varga, Viktor and Zelena, Dóra and Freund, Tamás and Nyíri, Gábor},
	doi = {10.1126/science.aay8746},
	journal-iso = {SCIENCE},
	journal = {SCIENCE},
	volume = {366},
	unique-id = {30881269},
	issn = {0036-8075},
	abstract = {Adverse events need to be quickly evaluated and memorized, yet how these processes are coordinated is poorly understood. We discovered a large population of excitatory neurons in mouse median raphe region (MRR) expressing vesicular glutamate transporter 2 (vGluT2) that received inputs from several negative experience–related brain centers, projected to the main aversion centers, and activated the septohippocampal system pivotal for learning of adverse events. These neurons were selectively activated by aversive but not rewarding stimuli. Their stimulation induced place aversion, aggression, depression-related anhedonia, and suppression of reward-seeking behavior and memory acquisition–promoting hippocampal theta oscillations. By contrast, their suppression impaired both contextual and cued fear memory formation. These results suggest that MRR vGluT2 neurons are crucial for the acquisition of negative experiences and may play a central role in depression-related mood disorders. © 2019 American Association for the Advancement of Science. All rights reserved.},
	year = {2019},
	eissn = {1095-9203},
	orcid-numbers = {Gulyás, Attila/0000-0003-4961-636X}
}

@article{MTMT:30725513,
	title = {Brainstem nucleus incertus controls contextual memory formation},
	url = {https://m2.mtmt.hu/api/publication/30725513},
	author = {Szőnyi, András and Sós, Katalin Eszter and Nyilas, Rita and Schlingloff, Dániel and Domonkos, Andor and Tresóné Takács, Virág and Pósfai, Balázs and Hegedüs, Panna and Priestley, James B. and Gundlach, Andrew L. and Gulyás, Attila and Varga, Viktor and Losonczy, Attila and Freund, Tamás and Nyíri, Gábor},
	doi = {10.1126/science.aaw0445},
	journal-iso = {SCIENCE},
	journal = {SCIENCE},
	volume = {364},
	unique-id = {30725513},
	issn = {0036-8075},
	abstract = {Hippocampal pyramidal cells encode memory engrams, which guide adaptive behavior. Selection of engram-forming cells is regulated by somatostatin-positive dendrite-targeting interneurons, which inhibit pyramidal cells that are not required for memory formation. Here, we found that gamma-aminobutyric acid ( GABA)-releasing neurons of the mouse nucleus incertus (NI) selectively inhibit somatostatin-positive interneurons in the hippocampus, both monosynaptically and indirectly through the inhibition of their subcortical excitatory inputs. We demonstrated that NI GABAergic neurons receive monosynaptic inputs from brain areas processing important environmental information, and their hippocampal projections are strongly activated by salient environmental inputs in vivo. Optogenetic manipulations of NI GABAergic neurons can shift hippocampal network state and bidirectionally modify the strength of contextual fear memory formation. Our results indicate that brainstem NI GABAergic cells are essential for controlling contextual memories.},
	year = {2019},
	eissn = {1095-9203},
	orcid-numbers = {Nyilas, Rita/0000-0002-9634-9535; Tresóné Takács, Virág/0000-0002-3276-4131; Pósfai, Balázs/0000-0003-1035-565X; Hegedüs, Panna/0000-0002-9984-5729; Gulyás, Attila/0000-0003-4961-636X}
}

@article{MTMT:30339603,
	title = {Interleukin-1 mediates ischaemic brain injury via distinct actions on endothelial cells and cholinergic neurons},
	url = {https://m2.mtmt.hu/api/publication/30339603},
	author = {Wong, Raymond and Lénárt, Nikolett and Hill, Laura and Toms, Lauren and Coutts, Graham and Martinecz, Bernadett and Császár, Eszter and Nyíri, Gábor and Papaemmanouil, Athina and Waisman, Ari and Müller, Werner and Schwaninger, Markus and Rothwell, Nancy and Francis, Sheila and Pinteaux, Emmanuel and Dénes, Ádám and Allan, Stuart M.},
	doi = {10.1016/j.bbi.2018.11.012},
	journal-iso = {BRAIN BEHAV IMMUN},
	journal = {BRAIN BEHAVIOR AND IMMUNITY},
	volume = {76},
	unique-id = {30339603},
	issn = {0889-1591},
	abstract = {The cytokine interleukin-1 (IL-1) is a key contributor to neuroinflammation and brain injury, yet mechanisms by which IL-1 triggers neuronal injury remain unknown. Here we induced conditional deletion of IL-1R1 in brain endothelial cells, neurons and blood cells to assess site-specific IL-1 actions in a model of cerebral ischaemia in mice. Tamoxifen treatment of IL-1R1 floxed (fl/fl) mice crossed with mice expressing tamoxifen-inducible Cre-recombinase under the Slco1c1 promoter resulted in brain endothelium-specific deletion of IL-1R1 and a significant decrease in infarct size (29%), blood-brain barrier (BBB) breakdown (53%) and neurological deficit (40%) compared to vehicle-treated or control (IL-1R1fl/fl) mice. Absence of brain endothelial IL-1 signalling improved cerebral blood flow, followed by reduced neutrophil infiltration and vascular activation 24 h after brain injury. Conditional IL-1R1 deletion in neurons using tamoxifen inducible nestin-Cre mice resulted in reduced neuronal injury (25%) and altered microglia-neuron interactions, without affecting cerebral perfusion or vascular activation. Deletion of IL-1R1 specifically in cholinergic neurons reduced infarct size, brain oedema and improved functional outcome. Ubiquitous deletion of IL-1R1 had no effect on brain injury, suggesting beneficial compensatory mechanisms on other cells against the detrimental effects of IL-1 on endothelial cells and neurons. We also show that IL-1R1 signalling deletion in platelets or myeloid cells does not contribute to brain injury after experimental stroke. Thus, brain endothelial and neuronal (cholinergic) IL-1R1 mediate detrimental actions of IL-1 in the brain in ischaemic stroke. Cell-specific targeting of IL-1R1 in the brain could therefore have therapeutic benefits in stroke and other cerebrovascular diseases.},
	year = {2019},
	eissn = {1090-2139},
	pages = {126-138},
	orcid-numbers = {Lénárt, Nikolett/0000-0002-7456-949X; Toms, Lauren/0000-0002-7456-949X; Császár, Eszter/0000-0002-5543-4100; Waisman, Ari/0000-0003-1058-0515; Schwaninger, Markus/0000-0003-4304-8234; Francis, Sheila/0000-0002-1297-9725}
}

@article{MTMT:3348809,
	title = {Chronic Amyloid beta Oligomer Infusion Evokes Sustained Inflammation and Microglial Changes in the Rat Hippocampus via NLRP3.},
	url = {https://m2.mtmt.hu/api/publication/3348809},
	author = {Fekete, Csaba and Vastagh, Csaba and Dénes, Ádám and Hrabovszky, Erik and Nyíri, Gábor and Kalló, Imre and Liposits, Zsolt and Sárvári, Miklós},
	doi = {10.1016/j.neuroscience.2018.02.046},
	journal-iso = {NEUROSCIENCE},
	journal = {NEUROSCIENCE},
	volume = {405},
	unique-id = {3348809},
	issn = {0306-4522},
	abstract = {Microglia are instrumental for recognition and elimination of amyloid beta1-42 oligomers (AbetaOs), but the long-term consequences of AbetaO-induced inflammatory changes in the brain are unclear. Here, we explored microglial responses and transciptome-level inflammatory signatures in the rat hippocampus after chronic AbetaO challenge. Middle-aged Long Evans rats received intracerebroventricular infusion of AbetaO or vehicle for 4weeks, followed by treatment with artificial CSF or MCC950 for the subsequent 4weeks. AbetaO infusion evoked a sustained inflammatory response including activation of NF-kappaB, triggered microglia activation and increased the expression of pattern recognition and phagocytic receptors. Abeta1-42 plaques were not detectable likely due to microglial elimination of infused oligomers. In addition, we found upregulation of neuronal inhibitory ligands and their cognate microglial receptors, while downregulation of Esr1 and Scn1a, encoding estrogen receptor alpha and voltage-gated sodium-channel Na(v)1.1, respectively, was observed. These changes were associated with impaired hippocampus-dependent spatial memory and resembled early neurological changes seen in Alzheimer's disease. To investigate the role of inflammatory actions in memory deterioration, we performed MCC950 infusion, which specifically blocks the NLRP3 inflammasome. MCC950 attenuated AbetaO-evoked microglia reactivity, restored expression of neuronal inhibitory ligands, reversed downregulation of ERalpha, and abolished memory impairments. Furthermore, MCC950 abrogated AbetaO-invoked reduction of serum IL-10. These findings provide evidence that in response to AbetaO infusion microglia change their phenotype, but the resulting inflammatory changes are sustained for at least one month after the end of AbetaO challenge. Lasting NLRP3-driven inflammatory alterations and altered hippocampal gene expression contribute to spatial memory decline.},
	keywords = {hippocampus; spatial memory; microglia; Estrogen receptors; NLRP3-inflammasome; amyloid β(1–42) oligomer},
	year = {2019},
	eissn = {1873-7544},
	pages = {35-46},
	orcid-numbers = {Vastagh, Csaba/0000-0002-5008-0999; Liposits, Zsolt/0000-0002-3508-2750}
}

@article{MTMT:3406802,
	title = {Differential Roles of the Two Raphe Nuclei in Amiable Social Behavior and Aggression - An Optogenetic Study},
	url = {https://m2.mtmt.hu/api/publication/3406802},
	author = {Balázsfi, Diána and Zelena, Dóra and Demeter, Kornél and Miskolczi, Christina and Varga, Zoltán Kristóf and Nagyvaradi, A and Nyíri, Gábor and Cserép, Csaba and Baranyi, Mária and Sperlágh, Beáta and Haller, József},
	doi = {10.3389/fnbeh.2018.00163},
	journal-iso = {FRONT BEHAV NEUROSCI},
	journal = {FRONTIERS IN BEHAVIORAL NEUROSCIENCE},
	volume = {12},
	unique-id = {3406802},
	abstract = {Serotonergic mechanisms hosted by raphe nuclei have important roles in affiliative and agonistic behaviors but the separate roles of the two nuclei are poorly understood. Here we studied the roles of the dorsal (DR) and median raphe region (MRR) in aggression by optogenetically stimulating the two nuclei. Mice received three 3 min-long stimulations, which were separated by non-stimulation periods of 3 min. The stimulation of the MRR decreased aggression in a phasic-like manner. Effects were rapidly expressed during stimulations, and vanished similarly fast when stimulations were halted. No carryover effects were observed in the subsequent three trials performed at 2-day intervals. No effects on social behaviors were observed. By contrast, DR stimulation rapidly and tonically promoted social behaviors: effects were present during both the stimulation and non-stimulation periods of intermittent stimulations. Aggressive behaviors were marginally diminished by acute DR stimulations, but repeated stimulations administered over 8 days considerably decreased aggression even in the absence of concurrent stimulations, indicating the emergence of carryover effects. No such effects were observed in the case of social behaviors. We also investigated stimulation-induced neurotransmitter release in the prefrontal cortex, a major site of aggression control. MRR stimulation rapidly but transiently increased serotonin release, and induced a lasting increase in glutamate levels. DR stimulation had no effect on glutamate, but elicited a lasting increase of serotonin release. Prefrontal serotonin levels remained elevated for at least 2 h subsequent to DR stimulations. The stimulation of both nuclei increased GABA release rapidly and transiently. Thus, differential behavioral effects of the two raphe nuclei were associated with differences in their neurotransmission profiles. These findings reveal a surprisingly strong behavioral task division between the two raphe nuclei, which was associated with a nucleus-specific neurotransmitter release in the prefrontal cortex.},
	keywords = {glutamate; SEROTONIN; GABA; Aggression; Dorsal raphe; Median raphe},
	year = {2018},
	eissn = {1662-5153},
	orcid-numbers = {Cserép, Csaba/0000-0001-5513-2471; Haller, József/0000-0003-4315-3026}
}