The Na+/K+-ATPase generically enables deterministic bursting in class I neurons by shearing the spike-onset bifurcation structure.

Slow brain rhythms, for example during slow-wave sleep or pathological conditions like seizures and spreading depolarization, can be accompanied by oscillations in extracellular potassium concentration. Such slow brain rhythms typically have a lower frequency than tonic action-potential firing. They are assumed to arise from network-level mechanisms, involving synaptic interactions and delays, or from intrinsically bursting neurons.

KCC2 reverse mode helps to clear postsynaptically released potassium at glutamatergic synapses.

Extracellular potassium [K] elevation during synaptic activity retrogradely modifies presynaptic release and astrocytic uptake of glutamate. Hence, local K clearance and replenishment mechanisms are crucial regulators of glutamatergic transmission and plasticity. Based on recordings of astrocytic inward rectifier potassium current I and K-sensitive electrodes as sensors of [K] as well as on in silico modeling, we demonstrate that the neuronal K-Cl co-transporter KCC2 clears local perisynaptic [K] during synaptic excitation by operating in an activity-dependent reversed mode.