Topic: febrile seizures

To understand neural computation and the dynamics in the brain, we usually focus on the connectivity among neurons. In contrast, the properties of single neurons are often thought to be negligible, at least as far as the activity of networks is concerned. In this talk, I will contradict this notion and demonstrate how the biophysics of action-potential generation can have a decisive impact on network behaviour. Our recent theoretical work shows that, among regularly firing neurons, the somewhat unattended homoclinic type (characterized by a spike onset via a saddle homoclinic orbit bifurcation

The origins, mechanisms and consequences of epilepsy in the developing brain are incompletely understood. Many developmental epilepsies have a genetic basis and their mechanisms stem from deficits in the function of one or numerous genes. Others, such as those that follow prolonged febrile seizures or severe birth asphyxia in a ‘normal’ brain may depend on the interaction of the insult with the rapidly evolving brain cells and circuits. Yet, how early-life insults may provoke epilepsy is unclear, and requires multiple levels of analysis: behavior, circuits, cells [neurons, glia] and molecules.

To understand network computation, we usually focus on the connectivity among neurons. In this talk, however, I demonstrate how the biophysics of action-potential generation can have a decisive impact on network behaviour. Our recent theoretical work shows that, among regularly firing neurons, the less attended homoclinic type (characterized by a spike onset via a saddle homoclinic orbit bifurcation) particularly stands out: First, spikes of this type foster specific network states - synchronisation in inhibitory and splayed-out/frustrated states in excitatory networks. Second, homoclinic spik