TY  - JOUR
AU  - Chartrand, Thomas
AU  - Dalley, Rachel
AU  - Close, Jennie
AU  - Goriounova, Natalia A.
AU  - Lee, Brian R.
AU  - Mann, Rusty
AU  - Miller, Jeremy A.
AU  - Molnár, Gábor
AU  - Mukora, Alice
AU  - Alfiler, Lauren
AU  - Baker, Katherine
AU  - Bakken, Trygve E.
AU  - Berg, Jim
AU  - Bertagnolli, Darren
AU  - Braun, Thomas
AU  - Brouner, Krissy
AU  - Casper, Tamara
AU  - Csajbók, Éva
AU  - Dee, Nick
AU  - Egdorf, Tom
AU  - Enstrom, Rachel
AU  - Galakhova, Anna A.
AU  - Gary, Amanda
AU  - Gelfand, Emily
AU  - Goldy, Jeff
AU  - Hadley, Kristen
AU  - Heistek, Tim S.
AU  - Hill, DiJon
AU  - Jorstad, Nik
AU  - Kim, Lisa
AU  - Kocsis, Ágnes Katalin
AU  - Kruse, Lauren
AU  - Kunst, Michael
AU  - Leon, Gabriela
AU  - Long, Brian
AU  - Mallory, Matthew
AU  - McGraw, Medea
AU  - McMillen, Delissa
AU  - Melief, Erica J.
AU  - Mihut, Norbert
AU  - Ng, Lindsay
AU  - Nyhus, Julie
AU  - Oláh, Gáspár
AU  - Ozsvár, Attila
AU  - Omstead, Victoria
AU  - Péterfi, Zoltán Attila
AU  - Pom, Alice
AU  - Potekhina, Lydia
AU  - Rajanbabu, Ramkumar
AU  - Rózsa, Márton
AU  - Ruiz, Augustin
AU  - Sandle, Joanna Grace
AU  - Sunkin, Susan M.
AU  - Szöts, Ildikó
AU  - Tieu, Michael
AU  - Tóth, Martin
AU  - Trinh, Jessica
AU  - Vargas, Sara
AU  - Vumbaco, David
AU  - Williams, Grace
AU  - Wilson, Julia
AU  - Yao, Zizhen
AU  - Barzó, Pál
AU  - Cobbs, Charles
AU  - Ellenbogen, Richard G.
AU  - Esposito, Luke
AU  - Ferreira, Manuel
AU  - Gouwens, Nathan W.
AU  - Grannan, Benjamin
AU  - Gwinn, Ryder P.
AU  - Hauptman, Jason S.
AU  - Jarsky, Tim
AU  - Keene, C. Dirk
AU  - Ko, Andrew L.
AU  - Koch, Christof
AU  - Ojemann, Jeffrey G.
AU  - Patel, Anoop
AU  - Ruzevick, Jacob
AU  - Silbergeld, Daniel L.
AU  - Smith, Kimberly
AU  - Sorensen, Staci A.
AU  - Tasic, Bosiljka
AU  - Ting, Jonathan T.
AU  - Waters, Jack
AU  - de Kock, Christiaan P.J.
AU  - Mansvelder, Huib D.
AU  - Tamás, Gábor
AU  - Zeng, Hongkui
AU  - Kalmbach, Brian
AU  - Lein, Ed S.
TI  - Morphoelectric and transcriptomic divergence of the layer 1 interneuron repertoire in human versus mouse neocortex
JF  - SCIENCE
J2  - SCIENCE
VL  - 382
PY  - 2023
IS  - 6667
PG  - 19
SN  - 0036-8075
DO  - 10.1126/science.adf0805
UR  - https://m2.mtmt.hu/api/publication/34196545
ID  - 34196545
N1  - Allen Institute for Brain Science, Seattle, WA, United States            
            Center for Neurogenomics and Cognitive Research, Vrije Universiteit, Amsterdam, Netherlands            
            Research Group for Cortical Microcircuits of the Hungarian Academy of Science, University of Szeged, Szeged, Hungary            
            byte physics, Berlin, Germany            
            Department of Laboratory Medicine and Pathology, University of Washington, Seattle, WA, United States            
            Department of Neurosurgery, University of Szeged, Szeged, Hungary            
            Swedish Neuroscience Institute, Seattle, WA, United States            
            Department of Neurological Surgery, University of Washington, Seattle, WA, United States            
            Department of Physiology and Biophysics, University of Washington, Seattle, WA, United States            
            Washington National Primate Research Center, University of Washington, Seattle, WA, United States            
            Export Date: 10 November 2023; Cited By: 0
AB  - Neocortical layer 1 (L1) is a site of convergence between pyramidal-neuron dendrites and feedback axons where local inhibitory signaling can profoundly shape cortical processing. Evolutionary expansion of human neocortex is marked by distinctive pyramidal neurons with extensive L1 branching, but whether L1 interneurons are similarly diverse is underexplored. Using Patch-seq recordings from human neurosurgical tissue, we identified four transcriptomic subclasses with mouse L1 homologs, along with distinct subtypes and types unmatched in mouse L1. Subclass and subtype comparisons showed stronger transcriptomic differences in human L1 and were correlated with strong morphoelectric variability along dimensions distinct from mouse L1 variability. Accompanied by greater layer thickness and other cytoarchitecture changes, these findings suggest that L1 has diverged in evolution, reflecting the demands of regulating the expanded human neocortical circuit.
LA  - English
DB  - MTMT
ER  - 

TY  - JOUR
AU  - Rózsa, Márton
AU  - Tóth, Martin
AU  - Oláh, Gáspár
AU  - Baka, Judith
AU  - Lákovics, Rajmund
AU  - Barzó, Pál
AU  - Tamás, Gábor
TI  - Temporal disparity of action potentials triggered in axon initial segments and distal axons in the neocortex
JF  - SCIENCE ADVANCES
J2  - SCI ADV
VL  - 9
PY  - 2023
IS  - 41
PG  - 10
SN  - 2375-2548
DO  - 10.1126/sciadv.ade4511
UR  - https://m2.mtmt.hu/api/publication/34196534
ID  - 34196534
AB  - Neural population activity determines the timing of synaptic inputs, which arrive to dendrites, cell bodies, and axon initial segments (AISs) of cortical neurons. Action potential initiation in the AIS (AIS-APs) is driven by input integration, and the phase preference of AIS-APs during network oscillations is characteristic to cell classes. Distal regions of cortical axons do not receive synaptic inputs, yet experimental induction protocols can trigger retroaxonal action potentials (RA-APs) in axons distal from the soma. We report spontaneously occurring RA-APs in human and rodent cortical interneurons that appear uncorrelated to inputs and population activity. Network-linked triggering of AIS-APs versus input-independent timing of RA-APs of the same interneurons results in disparate temporal contribution of a single cell to in vivo network operation through perisomatic and distal axonal firing.
LA  - English
DB  - MTMT
ER  - 

TY  - JOUR
AU  - Horváth, Edit
AU  - Bela, Krisztina
AU  - Kulman, Kitti
AU  - Faragó, Nóra
AU  - Riyazuddin, Riyazuddin
AU  - Gallé, Ágnes
AU  - Puskás, László
AU  - Csiszár, Jolán
TI  - Glutathione Transferases are Involved in Salicylic Acid-Induced Transcriptional Reprogramming
JF  - JOURNAL OF PLANT GROWTH REGULATION
J2  - J PLANT GROWTH REGUL
VL  - 42
PY  - 2023
IS  - 7
SP  - 4497
EP  - 4510
PG  - 14
SN  - 0721-7595
DO  - 10.1007/s00344-023-10915-2
UR  - https://m2.mtmt.hu/api/publication/33647921
ID  - 33647921
N1  - Funding Agency and Grant Number: University of Szeged; Hungarian National Research, Development and Innovation Office [NKFIH K 125265, PD 131884, PD 131909]; University of Szeged Open Access Fund [5796]
            Funding text: Open access funding provided by University of Szeged. This study was supported by the Hungarian National Research, Development and Innovation Office [Grant Numbers: NKFIH K 125265, PD 131884, and PD 131909]. OA was supported by the University of Szeged Open Access Fund, Grant Number: 5796.
AB  - Salicylic acid (SA) plays a crucial role not only in defence against pathogen attacks, but also in abiotic stress responses. Recently, some key steps of SA signalling outlined the importance of redox state-dependent processes. This study explores the role of glutathione transferases (GSTs) in the transcriptional reprogramming of redox status-related genes in seven-day-old wild type and Atgst mutant Arabidopsis thaliana plants. The timing of redox changes, detected by the redox-sensitive green fluorescent protein (roGFP2), differed in wild type roots treated with 10 μM or 100 μM SA. Our results verified how the applied SA concentrations had different effect on the expression of oxidative stress- and redox-related genes, among them on the expression of AtGSTF8 and AtGSTU19 genes. Lower vitality and less negative E GSH values were specific characteristics of the Atgst mutants compared to the wild type plants throughout the experiment. Changes in the redox potential were only modest in the mutants after SA treatments. A slightly modified gene expression pattern was observed in control conditions and after 1 h of SA treatments in Atgst mutants compared to Col-0 roots. These data originating from the whole roots provide indirect evidence for the role of the investigated AtGSTF8 and AtGSTU19 isoenzymes in the transduction of the redox signal. Our results demonstrate that the investigated Arabidopsis GSTs have a role in maintaining the levels of reactive oxygen species- and redox homeostasis and are involved in transcriptional reprogramming in the roots.
LA  - English
DB  - MTMT
ER  - 

TY  - JOUR
AU  - Szegedi, Viktor
AU  - Bakos , Emőke
AU  - Furdan, Szabina
AU  - H. Kovács, Bálint Barna
AU  - Varga, Dániel
AU  - Erdélyi, Miklós
AU  - Barzó, Pál
AU  - Szűcs, Attila
AU  - Tamás, Gábor
AU  - Lamsa, Karri
TI  - HCN channels at the cell soma ensure the rapid electrical reactivity of fast-spiking interneurons in human neocortex
JF  - PLOS BIOLOGY
J2  - PLOS BIOL
VL  - 21
PY  - 2023
IS  - 2
PG  - 33
SN  - 1544-9173
DO  - 10.1371/journal.pbio.3002001
UR  - https://m2.mtmt.hu/api/publication/33644822
ID  - 33644822
N1  - Department of Physiology, Anatomy and Neuroscience, University of Szeged, Szeged, Hungary            
            Hungarian Centre of Excellence for Molecular Medicine Research Group for Human neuron physiology and therapy, Szeged, Hungary            
            Department of Optics and Quantum Electronics, University of Szeged, Szeged, Hungary            
            Department of Neurosurgery, University of Szeged, Szeged, Hungary            
            Neuronal Cell Biology Research Group, Eötvös Loránd University, Budapest, Budapest, Hungary            
            MTA-SZTE Research Group for Cortical Microcircuits, Department of Physiology, Anatomy and Neuroscience, University of Szeged, Szeged, Hungary            
            Export Date: 26 May 2023            
            CODEN: PBLIB            
            Correspondence Address: Lamsa, K.; Department of Physiology, Hungary; email: klamsa@bio.u-szeged.hu
AB  - Accumulating evidence indicates that there are substantial species differences in the properties of mammalian neurons, yet theories on circuit activity and information processing in the human brain are based heavily on results obtained from rodents and other experimental animals. This knowledge gap may be particularly important for understanding the neocortex, the brain area responsible for the most complex neuronal operations and showing the greatest evolutionary divergence. Here, we examined differences in the electrophysiological properties of human and mouse fast-spiking GABAergic basket cells, among the most abundant inhibitory interneurons in cortex. Analyses of membrane potential responses to current input, pharmacologically isolated somatic leak currents, isolated soma outside-out patch recordings, and immunohistochemical staining revealed that human neocortical basket cells abundantly express hyperpolarization-activated cyclic nucleotide-gated cation (HCN) channel isoforms HCN1 and HCN2 at the cell soma membrane, whereas these channels are sparse at the rodent basket cell soma membrane. Antagonist experiments showed that HCN channels in human neurons contribute to the resting membrane potential and cell excitability at the cell soma, accelerate somatic membrane potential kinetics, and shorten the lag between excitatory postsynaptic potentials and action potential generation. These effects are important because the soma of human fast-spiking neurons without HCN channels exhibit low persistent ion leak and slow membrane potential kinetics, compared with mouse fast-spiking neurons. HCN channels speed up human cell membrane potential kinetics and help attain an input–output rate close to that of rodent cells. Computational modeling demonstrated that HCN channel activity at the human fast-spiking cell soma membrane is sufficient to accelerate the input–output function as observed in cell recordings. Thus, human and mouse fast-spiking neurons exhibit functionally significant differences in ion channel composition at the cell soma membrane to set the speed and fidelity of their input–output function. These HCN channels ensure fast electrical reactivity of fast-spiking cells in human neocortex.
LA  - English
DB  - MTMT
ER  - 

TY  - JOUR
AU  - Berg, J.
AU  - Sorensen, S.A.
AU  - Ting, J.T.
AU  - Miller, J.A.
AU  - Chartrand, T.
AU  - Buchin, A.
AU  - Bakken, T.E.
AU  - Budzillo, A.
AU  - Dee, N.
AU  - Ding, S.-L.
AU  - Gouwens, N.W.
AU  - Hodge, R.D.
AU  - Kalmbach, B.
AU  - Lee, C.
AU  - Lee, B.R.
AU  - Alfiler, L.
AU  - Baker, K.
AU  - Barkan, E.
AU  - Beller, A.
AU  - Berry, K.
AU  - Bertagnolli, D.
AU  - Bickley, K.
AU  - Bomben, J.
AU  - Braun, T.
AU  - Brouner, K.
AU  - Casper, T.
AU  - Chong, P.
AU  - Crichton, K.
AU  - Dalley, R.
AU  - de, Frates R.
AU  - Desta, T.
AU  - Lee, S.D.
AU  - D’Orazi, F.
AU  - Dotson, N.
AU  - Egdorf, T.
AU  - Enstrom, R.
AU  - Farrell, C.
AU  - Feng, D.
AU  - Fong, O.
AU  - Furdan, Szabina
AU  - Galakhova, A.A.
AU  - Gamlin, C.
AU  - Gary, A.
AU  - Glandon, A.
AU  - Goldy, J.
AU  - Gorham, M.
AU  - Goriounova, N.A.
AU  - Gratiy, S.
AU  - Graybuck, L.
AU  - Gu, H.
AU  - Hadley, K.
AU  - Hansen, N.
AU  - Heistek, T.S.
AU  - Henry, A.M.
AU  - Heyer, D.B.
AU  - Hill, D.J.
AU  - Hill, C.
AU  - Hupp, M.
AU  - Jarsky, T.
AU  - Kebede, S.
AU  - Keene, L.
AU  - Kim, L.
AU  - Kim, M.-H.
AU  - Kroll, M.
AU  - Latimer, C.
AU  - Levi, B.P.
AU  - Link, K.E.
AU  - Mallory, M.
AU  - Mann, R.
AU  - Marshall, D.
AU  - Maxwell, M.
AU  - McGraw, M.
AU  - McMillen, D.
AU  - Melief, E.
AU  - Mertens, E.J.
AU  - Mezei, L.
AU  - Mihut, Norbert
AU  - Mok, S.
AU  - Molnár, Gábor
AU  - Mukora, A.
AU  - Ng, L.
AU  - Ngo, K.
AU  - Nicovich, P.R.
AU  - Nyhus, J.
AU  - Oláh, Gáspár
AU  - Oldre, A.
AU  - Omstead, V.
AU  - Ozsvár, Attila
AU  - Park, D.
AU  - Peng, H.
AU  - Pham, T.
AU  - Pom, C.A.
AU  - Potekhina, L.
AU  - Rajanbabu, R.
AU  - Ransford, S.
AU  - Reid, D.
AU  - Rimorin, C.
AU  - Ruiz, A.
AU  - Sandman, D.
AU  - Sulc, J.
AU  - Sunkin, S.M.
AU  - Szafer, A.
AU  - Szemenyei, Viktor
AU  - Thomsen, E.R.
AU  - Tieu, M.
AU  - Torkelson, A.
AU  - Trinh, J.
AU  - Tung, H.
AU  - Wakeman, W.
AU  - Waleboer, F.
AU  - Ward, K.
AU  - Wilbers, R.
AU  - Williams, G.
AU  - Yao, Z.
AU  - Yoon, J.-G.
AU  - Anastassiou, C.
AU  - Arkhipov, A.
AU  - Barzó, Pál
AU  - Bernard, A.
AU  - Cobbs, C.
AU  - de, Witt Hamer P.C.
AU  - Ellenbogen, R.G.
AU  - Esposito, L.
AU  - Ferreira, M.
AU  - Gwinn, R.P.
AU  - Hawrylycz, M.J.
AU  - Hof, P.R.
AU  - Idema, S.
AU  - Jones, A.R.
AU  - Keene, C.D.
AU  - Ko, A.L.
AU  - Murphy, G.J.
AU  - Ng, L.
AU  - Ojemann, J.G.
AU  - Patel, A.P.
AU  - Phillips, J.W.
AU  - Silbergeld, D.L.
AU  - Smith, K.
AU  - Tasic, B.
AU  - Yuste, R.
AU  - Segev, I.
AU  - de, Kock C.P.J.
AU  - Mansvelder, H.D.
AU  - Tamás, Gábor
AU  - Zeng, H.
AU  - Koch, C.
AU  - Lein, E.S.
TI  - Human neocortical expansion involves glutamatergic neuron diversification
JF  - NATURE
J2  - NATURE
VL  - 598
PY  - 2021
IS  - 7879
SP  - 151
EP  - 158
PG  - 8
SN  - 0028-0836
DO  - 10.1038/s41586-021-03813-8
UR  - https://m2.mtmt.hu/api/publication/32467760
ID  - 32467760
N1  - Allen Institute for Brain Science, Seattle, WA, United States            
            Department of Physiology and Biophysics, University of Washington, Seattle, WA, United States            
            Department of Pathology, University of Washington, Seattle, WA, United States            
            byte physics, Berlin, Germany            
            MTA-SZTE Research Group for Cortical Microcircuits, Department of Physiology, Anatomy, and Neuroscience, University of Szeged, Szeged, Hungary            
            Department of Integrative Neurophysiology, Center for Neurogenomics and Cognitive Research (CNCR), Vrije Universiteit, Amsterdam, Netherlands            
            Swedish Neuroscience Institute, Seattle, WA, United States            
            Department of Neurosurgery, University of Szeged, Szeged, Hungary            
            Cancer Center Amsterdam, Brain Tumor Center, Department of Neurosurgery, Amsterdam UMC, Vrije Universiteit, Amsterdam, Netherlands            
            Department of Neurological Surgery, University of Washington, Seattle, WA, United States            
            Nash Family Department of Neuroscience and Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, NY, United States            
            NeuroTechnology Center, Columbia University, New York, NY, United States            
            Edmond and Lily Safra Center for Brain Sciences and Department of Neurobiology, The Hebrew University Jerusalem, Jerusalem, Israel            
            Cited By :1            
            Export Date: 26 October 2021            
            CODEN: NATUA            
            Correspondence Address: Lein, E.S.; Allen Institute for Brain ScienceUnited States; email: Edl@alleninstitute.org
LA  - English
DB  - MTMT
ER  - 

TY  - JOUR
AU  - Wang, Kai-Yi
AU  - Wu, Jei-Wei
AU  - Cheng, Jen-Kun
AU  - Chen, Chun-Chung
AU  - Wong, Wai-Yi
AU  - Averkin, Róbert
AU  - Tamás, Gábor
AU  - Nakazawa, Kazu
AU  - Lien, Cheng-Chang
TI  - Elevation of hilar mossy cell activity suppresses hippocampal excitability and avoidance behavior
JF  - CELL REPORTS
J2  - CELL REP
VL  - 36
PY  - 2021
IS  - 11
PG  - 19
SN  - 2211-1247
DO  - 10.1016/j.celrep.2021.109702
UR  - https://m2.mtmt.hu/api/publication/32250210
ID  - 32250210
N1  - Funding Agency and Grant Number: Brain Research Center, National Yang Ming Chiao Tung University from the Featured Areas Research Center Program; Ministry of Science and Technology (MOST) in TaiwanMinistry of Science and Technology, Taiwan [106-2320-B-010-011-MY3, 106-2923-B-010-001-MY3, 108-2923-B-010001-MY2, 108-2911-I-010-504, 108-2321-B-010-009-MY2, 108-2320-B010-026-MY3, 108-2638-B-010-002-MY2, 110-2321-B-010-006, 105-2911-I-010-508]; National Health Research InstitutesNational Health Research Institutes, Japan [NHRI-EX110-10814NI]
            Funding text: We thank F. Ferraguti (University of Innsbruck, Austria), A. Dominique (University of Liege, Belgium), H.J. Cheng (Academia Sinica, Taiwan), H. Lu (George Washington University, USA), C.H. Wang (RIKEN, Japan), and J. Song (University of North Carolina, USA) for commenting on an earlier version of the manuscript, and all of the members of the Lien lab for insightful discussions. This work was financially supported by the Brain Research Center, National Yang Ming Chiao Tung University from the Featured Areas Research Center Program within the framework of the Higher Education Sprout Project by the Ministry of Education in Taiwan, National Health Research Institutes (NHRI-EX110-10814NI), and the Ministry of Science and Technology (MOST; 106-2320-B-010-011-MY3, 106-2923-B-010-001-MY3, 108-2923-B-010001-MY2, 108-2911-I-010-504, 108-2321-B-010-009-MY2, 108-2320-B010-026-MY3, 108-2638-B-010-002-MY2, 110-2321-B-010-006, MOSTHAS Project-based Personnel Exchange Program 105-2911-I-010-508) in Taiwan.
AB  - Modulation of hippocampal dentate gyrus (DG) excitability regulates anxiety. In the DG, glutamatergic mossy cells (MCs) receive the excitatory drive from principal granule cells (GCs) and mediate the feedback excitation and inhibition of GCs. However, the circuit mechanism by which MCs regulate anxiety-related information routing through hippocampal circuits remains unclear. Moreover, the correlation between MC activity and anxiety states is unclear. In this study, we first demonstrate, by means of calcium fiber photometry, that MC activity in the ventral hippocampus (vHPC) of mice increases while they explore anxiogenic environments. Next, juxtacellular recordings reveal that optogenetic activation of MCs preferentially recruits GABAergic neurons, thereby suppressing GCs and ventral CA1 neurons. Finally, chemogenetic excitation of MCs in the vHPC reduces avoidance behaviors in both healthy and anxious mice. These results not only indicate an anxiolytic role of MCs but also suggest that MCs may be a potential therapeutic target for anxiety disorders.
LA  - English
DB  - MTMT
ER  - 

TY  - JOUR
AU  - Ozsvár, Attila
AU  - Komlósi, Gergely
AU  - Oláh, Gáspár
AU  - Baka, Judith
AU  - Molnár, Gábor
AU  - Tamás, Gábor
TI  - Predominantly linear summation of metabotropic postsynaptic potentials follows coactivation of neurogliaform interneurons
JF  - ELIFE
J2  - ELIFE
VL  - 10
PY  - 2021
PG  - 25
SN  - 2050-084X
DO  - 10.7554/eLife.65634
UR  - https://m2.mtmt.hu/api/publication/32186919
ID  - 32186919
N1  - Funding Agency and Grant Number: Hungarian Science FoundationOrszagos Tudomanyos Kutatasi Alapprogramok (OTKA) [GINOP 2.3.2-15-2016-00018]; NRDI OfficeNational Research, Development & Innovation Office (NRDIO) - Hungary [OTKA K128863]; Hungarian Academy of Sciences Janos Bolyai Research Scholarship; Innovation and Technology Fund New National Excellence Program; Eotvos Lorand Research Network ELKH-SZTE Research Group for Cortical Microcircuits
            Funding text: Eo tvos Lorand Research Network ELKH-SZTE Research Group for Cortical Microcircuits Ga ' bor Tama; Hungarian Science Foundation GINOP 2.3.2-15-2016-00018 Ga ' bor Tamas; NRDI Office OTKA K128863 Gabor Molnar Gabor Tama; Hungarian Academy of Sciences Janos Bolyai Research Scholarship Ga ' bor Molna; Innovation and Technology Fund New National Excellence Program Ga ' bor Molna ' r
AB  - Summation of ionotropic receptor-mediated responses is critical in neuronal computation by shaping input-output characteristics of neurons. However, arithmetics of summation for metabotropic signals are not known. We characterized the combined ionotropic and metabotropic output of neocortical neurogliaform cells (NGFCs) using electrophysiological and anatomical methods in the rat cerebral cortex. These experiments revealed that GABA receptors are activated outside release sites and confirmed coactivation of putative NGFCs in superficial cortical layers in vivo. Triple recordings from presynaptic NGFCs converging to a postsynaptic neuron revealed sublinear summation of ionotropic GABA(A) responses and linear summation of metabotropic GABA(B) responses. Based on a model combining properties of volume transmission and distributions of all NGFC axon terminals, we predict that in 83% of cases one or two NGFCs can provide input to a point in the neuropil. We suggest that interactions of metabotropic GABAergic responses remain linear even if most superficial layer interneurons specialized to recruit GABA(B) receptors are simultaneously active.
LA  - English
DB  - MTMT
ER  - 

TY  - JOUR
AU  - Iacone, Yasmine
AU  - Morais, Tatiana P.
AU  - David, Francois
AU  - Delicata, Francis
AU  - Sandle, Joanna
AU  - Raffai, Tímea
AU  - Parri, Harri Rheinallt
AU  - Weisser, Johan Juhl
AU  - Bundgaard, Christoffer
AU  - Klewe, Ib Vestergaard
AU  - Tamás, Gábor
AU  - Thomsen, Morten Skott
AU  - Crunelli, Vincenzo
AU  - Lőrincz, László Magor
TI  - Systemic administration of ivabradine, a hyperpolarization-activated cyclic nucleotide-gated channel inhibitor, blocks spontaneous absence seizures
JF  - EPILEPSIA
J2  - EPILEPSIA
VL  - 62
PY  - 2021
IS  - 7
SP  - 1729
EP  - 1743
PG  - 15
SN  - 0013-9580
DO  - 10.1111/epi.16926
UR  - https://m2.mtmt.hu/api/publication/32037613
ID  - 32037613
N1  - Funding Agency and Grant Number: Wellcome TrustWellcome TrustEuropean Commission [91882]; Orszagos Tudomanyos Kutatasi AlapprogramokOrszagos Tudomanyos Kutatasi Alapprogramok (OTKA) [FK123831, NN125601]; Hungarian Brain Research Program [KTIA_NAP_13-2-2014-0014]; Ministry of Human Capacities, Hungary [20391-3/2018/FEKUSTRAT]; Marie Sklodowska-Curie Actions [H2020-MSCA-ITN-2016-722053]; Ester Floridia Neuroscience Research Foundation; Janos Bolyai FellowshipHungarian Academy of Sciences
            Funding text: Wellcome Trust, Grant/Award Number: 91882; Orszagos Tudomanyos Kutatasi Alapprogramok, Grant/Award Number: FK123831 and NN125601; Hungarian Brain Research Program, Grant/Award Number: KTIA_NAP_13-2-2014-0014; Ministry of Human Capacities, Hungary, Grant/Award Number: 20391-3/2018/FEKUSTRAT; Marie Sklodowska-Curie Actions, Grant/Award Number: H2020-MSCA-ITN-2016-722053; Ester Floridia Neuroscience Research Foundation; Magor L. Lorincz is a grantte of the Janos Bolyai Fellowship
AB  - Objective Hyperpolarization-activated cyclic nucleotide-gated (HCN) channels are known to be involved in the generation of absence seizures (ASs), and there is evidence that cortical and thalamic HCN channel dysfunctions may have a proabsence role. Many HCN channel blockers are available, but their role in ASs has been investigated only by localized brain injection or in in vitro model systems due to their limited brain availability. Here, we investigated the effect on ASs of orally administered ivabradine (an HCN channel blocker approved for the treatment of heart failure in humans) following injection of the P-glycoprotein inhibitor elacridar, which is known to increase penetration into the brain of drug substrates for this efflux transporter. The action of ivabradine was also tested following in vivo microinjection into the cortical initiation network (CIN) of the somatosensory cortex and in the thalamic ventrobasal nucleus (VB) as well as on cortical and thalamocortical neurons in brain slices. Methods We used electroencephalographic recordings in freely moving Genetic Absence Epilepsy Rats From Strasbourg (GAERSs) to assess the action of oral administration of ivabradine, with and without elacridar, on ASs. Ivabradine was also microinjected into the CIN and VB of GAERSs in vivo and applied to Wistar CIN and GAERS VB slices while recording patch-clamped cortical Layer 5/6 and thalamocortical neurons, respectively. Results Oral administration of ivabradine markedly and dose-dependently reduced ASs. Ivabradine injection into CIN abolished ASs and elicited small-amplitude 4-7-Hz waves (without spikes), whereas in the VB it was less potent. Moreover, ivabradine applied to GAERS VB and Wistar CIN slices selectively decreased HCN channel-dependent properties of cortical Layer 5/6 pyramidal and thalamocortical neurons, respectively. Significance These results provide the first demonstration of the antiabsence action of a systemically administered HCN channel blocker, indicating the potential of this class of drugs as a novel therapeutic avenue for ASs.
LA  - English
DB  - MTMT
ER  - 

TY  - JOUR
AU  - Molnár, Benedek
AU  - Sere, Péter
AU  - Bordé, Sándor
AU  - Koós, Krisztián
AU  - Zsigri, Nikolett
AU  - Horváth, Péter
AU  - Lőrincz, László Magor
TI  - Cell-Type Specific Arousal-Dependent Modulation of Thalamic Activity in the Lateral Geniculate Nucleus
JF  - CEREBRAL CORTEX COMMUNICATIONS
J2  - CEREB CORTEX COMMUN
VL  - 2
PY  - 2021
PG  - 9
SN  - 2632-7376
DO  - 10.1093/texcom/tgab020
UR  - https://m2.mtmt.hu/api/publication/31953949
ID  - 31953949
LA  - English
DB  - MTMT
ER  - 

TY  - JOUR
AU  - Yuste, Rafael
AU  - Hawrylycz, Michael
AU  - Aalling, Nadia
AU  - Aguilar-Valles, Argel
AU  - Arendt, Detlev
AU  - Arnedillo, Ruben Armananzas
AU  - Ascoli, Giorgio A.
AU  - Bielza, Concha
AU  - Bokharaie, Vahid
AU  - Bergmann, Tobias Borgtoft
AU  - Bystron, Irina
AU  - Capogna, Marco
AU  - Chang, Yoonjeung
AU  - Clemens, Ann
AU  - de, Kock Christiaan P. J.
AU  - DeFelipe, Javier
AU  - Dos, Santos Sandra Esmeralda
AU  - Dunville, Keagan
AU  - Feldmeyer, Dirk
AU  - Fiath, Richard
AU  - Fishell, Gordon James
AU  - Foggetti, Angelica
AU  - Gao, Xuefan
AU  - Ghaderi, Parviz
AU  - Goriounova, Natalia A.
AU  - Guentuerkuen, Onur
AU  - Hagihara, Kenta
AU  - Hall, Vanessa Jane
AU  - Helmstaedter, Moritz
AU  - Herculano, Suzana
AU  - Hilscher, Markus M.
AU  - Hirase, Hajime
AU  - Hjerling-Leffler, Jens
AU  - Hodge, Rebecca
AU  - Huang, Josh
AU  - Huda, Rafiq
AU  - Khodosevich, Konstantin
AU  - Kiehn, Ole
AU  - Koch, Henner
AU  - Kuebler, Eric S.
AU  - Kuhnemund, Malte
AU  - Larranaga, Pedro
AU  - Lelieveldt, Boudewijn
AU  - Louth, Emma Louise
AU  - Lui, Jan H.
AU  - Mansvelder, Huibert D.
AU  - Marin, Oscar
AU  - Martinez-Trujillo, Julio
AU  - Chameh, Homeira Moradi
AU  - Nath, Alok
AU  - Nedergaard, Maiken
AU  - Nemec, Pavel
AU  - Ofer, Netanel
AU  - Pfisterer, Ulrich Gottfried
AU  - Pontes, Samuel
AU  - Redmond, William
AU  - Rossier, Jean
AU  - Sanes, Joshua R.
AU  - Scheuermann, Richard
AU  - Serrano-Saiz, Esther
AU  - Steiger, Jochen F.
AU  - Somogyi, Peter
AU  - Tamás, Gábor
AU  - Tolias, Andreas Savas
AU  - Tosches, Maria Antonietta
AU  - Garcia, Miguel Turrero
AU  - Vieira, Hermany Munguba
AU  - Wozny, Christian
AU  - Wuttke, Thomas V.
AU  - Yong, Liu
AU  - Yuan, Juan
AU  - Zeng, Hongkui
AU  - Lein, Ed
TI  - A community-based transcriptomics classification and nomenclature of neocortical cell types (vol 23, pg 1456, 2020)
JF  - NATURE NEUROSCIENCE
J2  - NAT NEUROSCI
VL  - 24
PY  - 2021
IS  - 4
SP  - 613
EP  - 613
PG  - 1
SN  - 1097-6256
DO  - 10.1038/s41593-020-00768-3
UR  - https://m2.mtmt.hu/api/publication/31889143
ID  - 31889143
N1  - Funding Agency and Grant Number: NINDS NIH HHSUnited States Department of Health & Human ServicesNational Institutes of Health (NIH) - USANIH National Institute of Neurological Disorders & Stroke (NINDS) [R01 NS039600] Funding Source: Medline
LA  - English
DB  - MTMT
ER  -