title: Reduced synchronization persistence in neural networks derived from atm-deficient mice.
abstract: Many neurodegenerative diseases are characterized by malfunction of the DNA damage response. Therefore, it is important to understand the connection between system level neural network behavior and DNA. Neural networks drawn from genetically engineered animals, interfaced with micro-electrode arrays allowed us to unveil connections between networks' system level activity properties and such genome instability. We discovered that Atm protein deficiency, which in humans leads to progressive motor impairment, leads to a reduced synchronization persistence compared to wild type synchronization, after chemically imposed DNA damage. Not only do these results suggest a role for DNA stability in neural network activity, they also establish an experimental paradigm for empirically determining the role a gene plays on the behavior of a neural network.
authors.affiliation: George S. Wise Faculty of Life Sciences, Department of Neurobiology, Tel Aviv University Tel Aviv, Israel.
authors.forename: Noah
authors.initials: N
authors.lastname: Levine-Small
authors.forename: Ziv
authors.initials: Z
authors.lastname: Yekutieli
authors.forename: Jonathan
authors.initials: J
authors.lastname: Aljadeff
authors.forename: Stefano
authors.initials: S
authors.lastname: Boccaletti
authors.forename: Eshel
authors.initials: E
authors.lastname: Ben-Jacob
authors.forename: Ari
authors.initials: A
authors.lastname: Barzilai