Via the capacitance clamp, electrophysiologists can for the first time flexibly set an artificial membrane capacitance for neurons and other excitable cells and thereby adjust their membrane time constant independent of any conductance changes.

Independently gating ion channels typically act fast within milliseconds, but cooperative interactions within a cluster of channels allow for a memory of previous electrical activity for several seconds.

Structures of the replicative DNA polymerase Pol IIIα, the DNA sliding clamp, the proofreading exonuclease, and the processivity switch Tau (τ) suggest a mechanism for quick release during lagging strand synthesis.

Purkinje cell inputs onto cerebellar nuclei (CbN) neurons have highly variable strengths, which allow them to influence CbN firing in a graded manner, with the largest individual inputs effectively regulating both the rate and spike timing of CbN neuron firing.

A multi-scale integration of experimental and computational approaches shows how a non-linear dependence of T-type calcium channel gating on GABA_B receptor activity regulates thalamic network oscillations.

Customization of ion channel gating enhances homeostatic regulation through automatic detection and correction of abnormal physiological changes, as illustrated by self-restoration of excitation rhythm in cardiac arrhythmias.

Nuanced changes in the mechanism of oscillation in reciprocally inhibitory circuits can profoundly alter the circuit stability in response to perturbations and inputs.

Animal-to-animal variability in neural circuit elements is often hidden under normal conditions, but becomes functionally relevant when the system is challenged by injury.

No single molecular change is uniquely necessary to cause neuropathic changes in primary afferent excitability; multiple different changes are sufficient.

The location of impact sounds, common stimuli whose detection is crucial for survival, is encoded by a precise interaction between excitation and inhibition rather than coincidence detection of excitatory events.