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001-es BibID:BIBFORM097650
035-os BibID:(cikkazonosító)721773 (Scopus)85118322206
Első szerző:Somogyi Attila
Cím:Increased Signal Delays ad Unaltered Synaptic Input Pattern Recognitio in Layer III Neocortical Pyramidal Neurons of the rTg4510 Mouse Model of Tauopathy : a Computer Simulation Study With Passive Membrane / Attila Somogyi, Ervin Wolf
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Frontiers in Neuroscience. - 15 (2021), p. 721773. -
További szerzők:Wolf Ervin (1961-) (fizikus, neurobiológus)
Pályázati támogatás:TÁMOP 4.2.4. B/2-11-1-2012-0001
TÁMOP 4.2.4. A/2- 11-1-2012-0001
Internet cím:DOI
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001-es BibID:BIBFORM063917
Első szerző:Somogyi Attila
Cím:A novel form of compensation in the Tg2576 amyloid mouse model of Alzheimer disease / Attila Somogyi, Zoltán Katonai, Alán Alpár, Ervin Wolf
Megjegyzések:One century after its first description, pathology of Alzheimer's disease (AD) is still poorly44 understood. Amyloid-related dendritic atrophy and membrane alterations of susceptible brain45 neurons in AD, and in animal models of AD are widely recognized. However, little effort has46 been made to study the potential effects of combined morphological and membrane47 alterations on signal transfer and synaptic integration in neurons that build up affected neural48 networks in AD. In this study spatial reconstructions and electrophysiological measurements49 of layer II/III pyramidal neurons of the somatosensory cortex from wild-type (WT) and50 transgenic (TG) human amyloid precursor protein (hAPP) overexpressing Tg2576 mice were51 used to build faithful segmental cable models of these neurons. Local synaptic activities were52 simulated in various points of the dendritic arbors and properties of subthreshold dendritic53 impulse propagation and predictors of synaptic input pattern recognition ability were54 quantified and compared in modeled WT and TG neurons.55 Despite the widespread dendritic degeneration and membrane alterations in mutant mouse56 neurons, surprisingly little, or no change was detected in steady-state and 50Hz sinusoidal57 voltage transfers, current transfers, and local and propagation delays of PSPs travelling along58 dendrites of TG neurons. Synaptic input pattern recognition ability was also predicted to be59 unaltered in TG neurons in two different soma-dendritic membrane models investigated. Our60 simulations predict the way how subthreshold dendritic signaling and pattern recognition are61 preserved in TG neurons: Amyloid-related membrane alterations compensate for the62 pathological effects that dendritic atrophy has on subthreshold dendritic signal transfer and63 integration in layer II/III somatosensory neurons of this hAPP mouse model for AD. Since64 neither propagation of single PSPs nor integration of multiple PSPs (pattern recognition)65 changes in TG neurons, we conclude that AD-related neuronal hyperexcitability cannot be66 accounted for by altered subthreshold dendritic signaling in these neurons but67 hyperexcitability is related to changes in active membrane properties and network connectivity
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Alzheimer's disease
human amyloid precursor protein
computer 28 simulations
mouse somatosensory cortex
electrotonic analysis
29 conservation of dendritic signaling
synaptic integration
Megjelenés:Frontiers in Cellular Neuroscience. - 10 : 152 (2016), p. [38]. -
További szerzők:Katonai Zoltán Alpár Alán Wolf Ervin (1961-) (fizikus, neurobiológus)
Internet cím:Szerző által megadott URL
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