Search bioRxivSearch

Biology subjects

Christoph Kirst

Publications and source records attributed to Christoph Kirst.

2 recordsLinked to original sources

Dynamic information routing in complex networks

Abstract Flexible information routing fundamentally underlies the function of many biological and artificial networks. Yet, how such systems may specifically communicate and dynamically route information is not well understood. Here we identify a generic mechanism to route information on top of collective dynamical reference states in complex networks. Switching between collective dynamics induces flexible reorganization of information sharing and routing patterns, as quantified by delayed mutual information and transfer entropy measures between activities of a network's units. We demonstrate the power of this generic mechanism specifically for oscillatory dynamics and analyze how individual unit properties, the network topology and external inputs coact to systematically organize information routing. For multi-scale, modular architectures, we resolve routing patterns at all levels. Interestingly, local interventions within one sub-network may remotely determine non-local network-wide communication. These results help understanding and designing information routing patterns across systems where collective dynamics co-occurs with a communication function.

Neuroscience

Fundamental Structure and Modulation of Neuronal Excitability: Synaptic Control of Coding, Resonance, and Network Synchronization

Neuronal encoding and collective network activity depend on the precise mechanism for generating action potentials. A dynamic switch in this mechanism could greatly expand the functional repertoire of neurons and circuits. Here we show that changes in neuronal biophysics control a complex, yet fundamental, sequence of dynamic transitions in neuronal excitability in which neurons switch from integrators to resonators near the spike threshold, from simple voltage dynamics to the bistable co-existence of action potentials and quiescence, and from continuous class-I to discontinuous class-II firing rate encoding. Using multiple bifurcation theory, we prove that this transition sequence is universal in conductance-based neurons. Using dynamic-clamp and pharmacology, we show experimentally that an increase in leak conductance or application of the inhibitory agonist GABA can dynamically induce these transitions in hippocampal and brainstem neurons. Our results imply that synaptic activity can flexibly control resonance, excitability and bistability of neurons. In simulated neuronal networks, we show that such synaptically induced transitions provide a mechanism for the dynamic gating of input signals and the targeted synchronization of sub-networks with a tunable number of neurons.\n\nSignificanceNeuronal function depends on the mechanism by which neurons transform synaptic input into action potentials (APs). It is unclear how neurons might control the AP mechanism to systematically modulate their responses to input signals or their collective behavior. Here we identify a complex, but model-independent, universal sequence of transitions in the dynamics of AP generation. Using patch-clamp recordings, we show that synaptic receptor activation can flexibly change the AP dynamics, confirming our theoretical predictions: non-resonant neurons develop a sub-threshold resonance, become bistable, and develop an abrupt jump in onset AP frequency. Our results explain how synapses or neuro-modulators could control neuronal excitability, influence information processing, and processing during collective network dynamics.

Neuroscience