@article{MTMT:2940235,
	title = {Acute intracerebral treatment with amyloid-beta (1-42) alters the profile of neuronal oscillations that accompany LTP induction and results in impaired LTP in freely behaving rats},
	url = {https://m2.mtmt.hu/api/publication/2940235},
	author = {Kalweit, Alexander Nikolai and Yang, Honghong and Colitti-Klausnitzer, Jens and Fülöp, Lívia and Bozsó, Zsolt and Penke, Botond and Manahan-Vaughan, Denise},
	doi = {10.3389/fnbeh.2015.00103},
	journal-iso = {FRONT BEHAV NEUROSCI},
	journal = {FRONTIERS IN BEHAVIORAL NEUROSCIENCE},
	volume = {9},
	unique-id = {2940235},
	year = {2015},
	eissn = {1662-5153},
	orcid-numbers = {Fülöp, Lívia/0000-0002-8010-0129; Bozsó, Zsolt/0000-0002-5713-3096; Penke, Botond/0000-0003-0938-0567}
}

@article{MTMT:2812783,
	title = {Amyloid-β1-42 disrupts synaptic plasticity by altering glutamate recycling at the synapse},
	url = {https://m2.mtmt.hu/api/publication/2812783},
	author = {Varga, Edina and Juhász, Gábor and Bozsó, Zsolt and Penke, Botond and Fülöp, Lívia and Szegedi, Viktor},
	doi = {10.3233/JAD-142367},
	journal-iso = {J ALZHEIMERS DIS},
	journal = {JOURNAL OF ALZHEIMER'S DISEASE},
	volume = {45},
	unique-id = {2812783},
	issn = {1387-2877},
	abstract = {Alzheimer's disease (AD) is the most prevalent form of neurodegenerative disorders characterized by neuritic plaques containing amyloid-beta peptide (Abeta) and neurofibrillary tangles. Evidence has been reported that Abeta1-42 plays an essential pathogenic role in decreased spine density, impairment of synaptic plasticity, and neuronal loss with disruption of memory-related synapse function, all associated with AD. Experimentally, Abeta1-42 oligomers perturb hippocampal long-term potentiation (LTP), an electrophysiological correlate of learning and memory. Abeta was also reported to perturb synaptic glutamate (Glu)-recycling by inhibiting excitatory-amino-acid-transporters. Elevated level of extracellular Glu leads to activation of perisynaptic receptors, including NR2B subunit containing NMDARs. These receptors were shown to induce impaired LTP and enhanced long-term depression and proapoptotic pathways, all central features of AD. In the present study, we investigated the role of Glu-recycling on Abeta1-42-induced LTP deficit in the CA1. We found that Abeta-induced LTP damage, which was mimicked by the Glu-reuptake inhibitor TBOA, could be rescued by blocking the NR2B subunit of NMDA receptors. Furthermore, decreasing the level of extracellular Glu using a Glu scavenger also restores TBOA or Abeta induces LTP damage. Overall, these results suggest that reducing ambient Glu in the brain can be protective against Abeta-induced synaptic disruption.},
	keywords = {Brain; ARTICLE; MOUSE; priority journal; controlled study; nonhuman; animal tissue; animal model; animal experiment; LONG-TERM POTENTIATION; synapse; n methyl dextro aspartic acid receptor; glutamic acid; unclassified drug; Alzheimer's disease; aspartic acid; SCAVENGER; nerve cell plasticity; amyloid beta protein[1-42]; ifenprodil; long term potentiation; pyruvate sodium; dextro levo threo beta benzyloxyaspartate; TBOA; NR2B; glutamate-reuptake; glutamate scavenger},
	year = {2015},
	eissn = {1875-8908},
	pages = {449-456},
	orcid-numbers = {Bozsó, Zsolt/0000-0002-5713-3096; Penke, Botond/0000-0003-0938-0567; Fülöp, Lívia/0000-0002-8010-0129; Szegedi, Viktor/0000-0003-4191-379X}
}

@article{MTMT:2755870,
	title = {Abeta(1-42) Enhances Neuronal Excitability in the CA1 via NR2B Subunit-Containing NMDA Receptors},
	url = {https://m2.mtmt.hu/api/publication/2755870},
	author = {Varga, Edina and Juhász, Gábor and Bozsó, Zsolt and Penke, Botond and Fülöp, Lívia and Szegedi, Viktor},
	doi = {10.1155/2014/584314},
	journal-iso = {NEURAL PLAST},
	journal = {NEURAL PLASTICITY},
	volume = {2014},
	unique-id = {2755870},
	issn = {2090-5904},
	abstract = {Neuronal hyperexcitability is a phenomenon associated with early Alzheimer's disease. The underlying mechanism is considered to involve excessive activation of glutamate receptors; however, the exact molecular pathway remains to be determined. Extracellular recording from the CA1 of hippocampal slices is a long-standing standard for a range of studies both in basic research and in neuropharmacology. Evoked field potentials (fEPSPs) are regarded as the input, while spiking rate is regarded as the output of the neuronal network; however, the relationship between these two phenomena is not fully clear. We investigated the relationship between spontaneous spiking and evoked fEPSPs using mouse hippocampal slices. Blocking AMPA receptors (AMPARs) with CNQX abolished fEPSPs, but left firing rate unchanged. NMDA receptor (NMDAR) blockade with MK801 decreased neuronal spiking dose dependently without altering fEPSPs. Activating NMDARs by small concentration of NMDA induced a trend of increased firing. These results suggest that fEPSPs are mediated by synaptic activation of AMPARs, while spontaneous firing is regulated by the activation of extrasynaptic NMDARs. Synaptotoxic Abeta(1-42) increased firing activity without modifying evoked fEPSPs. This hyperexcitation was prevented by ifenprodil, an antagonist of the NR2B NMDARs. Overall, these results suggest that Abeta(1-42) induced neuronal overactivity is not dependent on AMPARs but requires NR2B.},
	year = {2014},
	eissn = {1687-5443},
	orcid-numbers = {Bozsó, Zsolt/0000-0002-5713-3096; Penke, Botond/0000-0003-0938-0567; Fülöp, Lívia/0000-0002-8010-0129; Szegedi, Viktor/0000-0003-4191-379X}
}

@article{MTMT:3050948,
	title = {Inhibitory interneuron deficit links altered network activity and cognitive dysfunction in Alzheimer model.},
	url = {https://m2.mtmt.hu/api/publication/3050948},
	author = {Verret, L and Mann, EO and Hang, GB and Barth, Albert and Cobos, I and Ho, K and Devidze, N and Masliah, E and Kreitzer, AC and Mody, I and Mucke, L and Palop, JJ},
	doi = {10.1016/j.cell.2012.02.046},
	journal-iso = {CELL},
	journal = {CELL},
	volume = {149},
	unique-id = {3050948},
	issn = {0092-8674},
	abstract = {Alzheimer's disease (AD) results in cognitive decline and altered network activity, but the mechanisms are unknown. We studied human amyloid precursor protein (hAPP) transgenic mice, which simulate key aspects of AD. Electroencephalographic recordings in hAPP mice revealed spontaneous epileptiform discharges, indicating network hypersynchrony, primarily during reduced gamma oscillatory activity. Because this oscillatory rhythm is generated by inhibitory parvalbumin (PV) cells, network dysfunction in hAPP mice might arise from impaired PV cells. Supporting this hypothesis, hAPP mice and AD patients had decreased levels of the interneuron-specific and PV cell-predominant voltage-gated sodium channel subunit Nav1.1. Restoring Nav1.1 levels in hAPP mice by Nav1.1-BAC expression increased inhibitory synaptic activity and gamma oscillations and reduced hypersynchrony, memory deficits, and premature mortality. We conclude that reduced Nav1.1 levels and PV cell dysfunction critically contribute to abnormalities in oscillatory rhythms, network synchrony, and memory in hAPP mice and possibly in AD.},
	keywords = {Animals; Humans; MICE; MEMORY; Mice, Inbred C57BL; Nerve Tissue Proteins/metabolism; learning; SYNAPSES; Mice, Transgenic; Disease Models, Animal; Neurons/metabolism; Hippocampus/metabolism; Sodium Channels/metabolism; Amyloid beta-Protein Precursor/metabolism; Interneurons/metabolism; Alzheimer Disease/*physiopathology; NAV1.1 Voltage-Gated Sodium Channel; In Vitro Techniques},
	year = {2012},
	eissn = {1097-4172},
	pages = {708-721}
}

@article{MTMT:246935,
	title = {Amyloid beta-Induced Neuronal Hyperexcitability Triggers Progressive Epilepsy},
	url = {https://m2.mtmt.hu/api/publication/246935},
	author = {Minkeviciene, R and Rheims, S and Dobszay, Márton Benedek and Zilberter, M and Hartikainen, J and Fülöp, Lívia and Penke, Botond and Zilberter, Y and Harkany, T and Pitkanen, A and Tanila, H},
	doi = {10.1523/JNEUROSCI.5215-08.2009},
	journal-iso = {J NEUROSCI},
	journal = {JOURNAL OF NEUROSCIENCE},
	volume = {29},
	unique-id = {246935},
	issn = {0270-6474},
	abstract = {Alzheimer's disease is associated with an increased risk of unprovoked seizures. However, the underlying mechanisms of seizure induction remain elusive. Here, we performed video-EEG recordings in mice carrying mutant human APPswe and PS1dE9 genes (APdE9 mice) and their wild-type littermates to determine the prevalence of unprovoked seizures. In two recording episodes at the onset of amyloid beta (A beta) pathogenesis (3 and 4.5 months of age), at least one unprovoked seizure was detected in 65% of APdE9 mice, of which 46% had multiple seizures and 38% had a generalized seizure. None of the wild-type mice had seizures. In a subset of APdE9 mice, seizure phenotype was associated with a loss of calbindin-D28k immunoreactivity in dentate granular cells and ectopic expression of neuropeptide Y in mossy fibers. In APdE9 mice, persistently decreased resting membrane potential in neocortical layer 2/3 pyramidal cells and dentate granule cells underpinned increased network excitability as identified by patch-clamp electrophysiology. At stimulus strengths evoking single-component EPSPs in wild-type littermates, APdE9 mice exhibited decreased action potential threshold and burst firing of pyramidal cells. Bath application (1h) of A beta 1-42 or A beta 25-35 (proto-) fibrils but not oligomers induced significant membrane depolarization of pyramidal cells and increased the activity of excitatory cell populations as measured by extracellular field recordings in the juvenile rodent brain, confirming the pathogenic significance of bath-applied A beta(proto-) fibrils. Overall, these data identify fibrillar A beta as a pathogenic entity powerfully altering neuronal membrane properties such that hyperexcitability of pyramidal cells culminates in epileptiform activity.},
	year = {2009},
	eissn = {1529-2401},
	pages = {3453-3462},
	orcid-numbers = {Fülöp, Lívia/0000-0002-8010-0129; Penke, Botond/0000-0003-0938-0567}
}

@article{MTMT:2086363,
	title = {Neuronal diversity and temporal dynamics: the unity of hippocampal circuit operations.},
	url = {https://m2.mtmt.hu/api/publication/2086363},
	author = {Klausberger, T and Somogyi, Péter Pál},
	doi = {10.1126/science.1149381},
	journal-iso = {SCIENCE},
	journal = {SCIENCE},
	volume = {321},
	unique-id = {2086363},
	issn = {0036-8075},
	abstract = {In the cerebral cortex, diverse types of neurons form intricate 
		circuits and cooperate in time for the processing and storage of 
		information. Recent advances reveal a spatiotemporal division 
		of labor in cortical circuits, as exemplified in the CA1 
		hippocampal area. In particular, distinct GABAergic (gamma-
		aminobutyric acid-releasing) cell types subdivide the surface of 
		pyramidal cells and act in discrete time windows, either on the 
		same or on different subcellular compartments. They also 
		interact with glutamatergic pyramidal cell inputs in a domain-
		specific manner and support synaptic temporal dynamics, network 
		oscillations, selection of cell assemblies, and the 
		implementation of brain states. The spatiotemporal 
		specializations in cortical circuits reveal that cellular 
		diversity and temporal dynamics coemerged during evolution, 
		providing a basis for cognitive behavior.},
	keywords = {Animals; Humans; Neurons/*physiology; Nerve Net/*physiology; Hippocampus/cytology/*physiology; Pyramidal Cells/*physiology; Synapses/physiology; cognition; Neural Pathways/physiology; Axons/physiology; gamma-Aminobutyric Acid/metabolism; Dendrites/physiology; Interneurons/*physiology; Biological Evolution},
	year = {2008},
	eissn = {1095-9203},
	pages = {53-57}
}

@article{MTMT:2138091,
	title = {Brain-state- and cell-type-specific firing of hippocampal interneurons in vivo.},
	url = {https://m2.mtmt.hu/api/publication/2138091},
	author = {Klausberger, T and Magill, PJ and Marton, LF and Roberts, JD and Cobden, PM and Buzsáki, György and Somogyi, Péter Pál},
	doi = {10.1038/nature01374},
	journal-iso = {NATURE},
	journal = {NATURE},
	volume = {421},
	unique-id = {2138091},
	issn = {0028-0836},
	abstract = {Neural-network oscillations at distinct frequencies have been implicated in the encoding, consolidation and retrieval of information in the hippocampus. Some GABA (gamma-aminobutyric acid)-containing interneurons fire phase-locked to theta oscillations (4-8 Hz) or to sharp-wave-associated ripple oscillations (120-200 Hz), which represent different behavioural states. Interneurons also entrain pyramidal cells in vitro. The large diversity of interneurons poses the question of whether they have specific roles in shaping distinct network activities in vivo. Here we report that three distinct interneuron types--basket, axo-axonic and oriens-lacunosum-moleculare cells--visualized and defined by synaptic connectivity as well as by neurochemical markers, contribute differentially to theta and ripple oscillations in anaesthetized rats. The firing patterns of individual cells of the same class are remarkably stereotyped and provide unique signatures for each class. We conclude that the diversity of interneurons, innervating distinct domains of pyramidal cells, emerged to coordinate the activity of pyramidal cells in a temporally distinct and brain-state-dependent manner.},
	keywords = {Animals; Male; RATS; Rats, Sprague-Dawley; Electrophysiology; Organ Specificity; Theta Rhythm/drug effects; gamma-Aminobutyric Acid/metabolism; *Anesthesia; Atropine/pharmacology; Pyramidal Cells/cytology/drug effects/physiology; Interneurons/*cytology/drug effects/*physiology; Hippocampus/*cytology/drug effects/*physiology; Consciousness/drug effects/physiology; Axons/drug effects/physiology; *Action Potentials/drug effects},
	year = {2003},
	eissn = {1476-4687},
	pages = {844-848}
}