Paradoxical signaling regulates structural plasticity in dendritic spines.

ABSTRACT: Transient spine enlargement (3- to 5-min timescale) is an important event associated with the structural plasticity of dendritic spines. Many of the molecular mechanisms associated with transient spine enlargement have been identified experimentally. Here, we use a systems biology approach to construct a mathematical model of biochemical signaling and actin-mediated transient spine expansion in response to calcium influx caused by NMDA receptor activation. We have identified that a key feature of this signaling network is the paradoxical signaling loop. Paradoxical components act bifunctionally in signaling networks, and their role is to control both the activation and the inhibition of a desired response function (protein activity or spine volume). Using ordinary differential equation (OD

SUBMITTER: Rangamani P 

PROVIDER: S-EPMC5018790 | biostudies-literature | 2016 Sep

REPOSITORIES: biostudies-literature