Reactive oxygen species regulate activity-dependent neuronal plasticity in .

Reactive oxygen species (ROS) have been extensively studied as damaging agents associated with ageing and neurodegenerative conditions. Their role in the nervous system under non-pathological conditions has remained poorly understood. Working with the larval locomotor network, we show that in neurons ROS act as obligate signals required for neuronal activity-dependent structural plasticity, of both pre- and postsynaptic terminals.

Regulation of motoneuron excitability and the setting of homeostatic limits.

Stability of neural circuits is reliant on homeostatic mechanisms that return neuron activity towards pre-determined and physiologically appropriate levels. Without these mechanisms, changes due to synaptic plasticity, ageing and disease may push neural circuits towards instability. Whilst widely documented, understanding of how and when neurons determine an appropriate activity level, the so-called set-point, remains unknown.

Selective modulation of chemical and electrical synapses of Helix neuronal networks during in vitro development.

Background: A large number of invertebrate models, including the snail Helix, emerged as particularly suitable tools for investigating the formation of synapses and the specificity of neuronal connectivity. Helix neurons can be individually identified and isolated in cell culture, showing well-conserved size, position, biophysical properties, synaptic connections, and physiological functions. Although we previously showed the potential usefulness of Helix polysynaptic circuits, a full characterization of synaptic connectivity and its dynamics during network development has not been performed.