@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}
}