http://www.cnr.it/ontology/cnr/individuo/prodotto/ID256635

Computational modeling of the effects of amyloid-beta on release probability at hippocampal synapses (Articolo in rivista)

Type

Prodotto della ricerca (Classe)
Articolo in rivista (Classe)

Label

Computational modeling of the effects of amyloid-beta on release probability at hippocampal synapses (Articolo in rivista) (literal)

Anno

2013-01-01T00:00:00+01:00 (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi

10.3389/fncom.2013.00001 (literal)

Alternative label

Romani A, Marchetti C, Bianchi D, Leinekugel X, Poirazi P, Migliore M, Marie H (2013)
Computational modeling of the effects of amyloid-beta on release probability at hippocampal synapses
in Frontiers in computational neuroscience; Frontiers Research Foundation, Lausanne (Swaziland)
(literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori

Romani A, Marchetti C, Bianchi D, Leinekugel X, Poirazi P, Migliore M, Marie H (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#url

http://www.frontiersin.org/Computational_Neuroscience/10.3389/fncom.2013.00001/abstract (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume

7 (literal)

Rivista

Frontiers in computational neuroscience (Rivista)

Note

ISI Web of Science (WOS) (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni

Laboratory of Molecular Mechanisms of Synaptic Plasticity, European Brain Research Institute, Rome, Italy Department of Physics, University La Sapienza, Rome, Italy Institut des Maladies Neurodégénératives, UMR 5293, CNRS and Université de Bordeaux, Bordeaux, France Institute of Molecular Biology and Biotechnology, Foundation of Research and Technology-Hellas, Heraklion, Crete, Greece Institute of Biophysics, National Research Council, Palermo, Italy (literal)

Titolo

Computational modeling of the effects of amyloid-beta on release probability at hippocampal synapses (literal)

Abstract

The role of amyloid beta (A?) in brain function and in the pathogenesis of Alzheimer's disease (AD) remains elusive. Recent publications reported that an increase in A? concentration perturbs pre-synaptic release in hippocampal neurons. In particular, it was shown in vitro that A? is an endogenous regulator of synaptic transmission at the CA3-CA1 synapse, enhancing its release probability. How this synaptic modulator influences neuronal output during physiological stimulation patterns, such as those elicited in vivo, is still unknown. Using a realistic model of hippocampal CA1 pyramidal neurons, we first implemented this A?-induced enhancement of release probability and validated the model by reproducing the experimental findings. We then demonstrated that this synaptic modification can significantly alter synaptic integration properties in a wide range of physiologically relevant input frequencies (from 5 to 200 Hz). Finally, we used natural input patterns, obtained from CA3 pyramidal neurons in vivo during free exploration of rats in an open field, to investigate the effects of enhanced A? on synaptic release under physiological conditions. The model shows that the CA1 neuronal response to these natural patterns is altered in the increased-A? condition, especially for frequencies in the theta and gamma ranges. These results suggest that the perturbation of release probability induced by increased A? can significantly alter the spike probability of CA1 pyramidal neurons and thus contribute to abnormal hippocampal function during AD. (literal)

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