@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}
}