Skin-associated bacteria underlie the production of a potent defensive neurotoxin in newts, impacting host physiology, molecular evolution, and predator-prey interactions in a coevolutionary arms race.

Visual impairment caused by monocular deprivation early in life can be reversed rapidly at older ages by temporarily blocking all activity in the non-deprived eye.

A human cellular model of a prototypical form of intractable childhood epilepsy supports selective impairment of inhibitory neurons as a key pathophysiological mechanism.

A-type fibroblast growth factor homologous factors generate resurgent currents in tetrodotoxin-resistant voltage-gated sodium channels, increase repetitive firing of sensory neurons, and provide a potentially important target for pain treatment strategies.

Herpes simplex virus reactivates from a latent infection when neurons become hyperexcitable in response to an inflammatory cytokine known to be released during fever and stress.

High-speed calcium imaging from the axon initial segment shows that sodium channels are in part permeable to calcium ions.

Feedback signaling between the synapse and nucleus via FGF22 and IGF2 directs the activity-dependent stabilization of presynaptic terminals in the mouse hippocampus.

Human sensory neurons may not only bridge a critical gap between drug discovery and clinical trials, but force a re-evaluation of basic assumptions about the mechanisms controlling primary afferent excitability.

A genetic strategy reveals that the perisynaptic glial response to neural activity in one population of these glia regulates postsynaptic function and therefore muscle fatigue.