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Electrophysiological and genetic analyses reveal a biophysical mechanism in parvalbumin interneurons, uncoupled from changes in gene expression, resulting in reduced cortical inhibition in early-stage Alzheimer's disease.

Polyunsaturated fatty acids facilitate or impede Kv7 channel activation, depending on channel subtype and their dominant functional site(s).

Loss of potassium channel activity from fast-spiking interneurons increases their excitability leading to unexpectedly increased fast excitatory transmission and seizure susceptibility.

Kiss1^ARH neurons transition from synchronous to burst firing under preovulatory levels of E2, causing a shift from peptidergic to glutamatergic transmission that drives the GnRH surge through enhanced glutamate neurotransmission.

The slow afterhyperpolarization that follows a burst of action potentials is a powerful regulator of neuronal excitability and is not due to IK1 (KCNN4), a member of the SK channel family.

Analysis of iconic and gating currents of wild type and mutated BK channels reveals a strong inhibition of this channel by extracellular acidification and elucidates the underlying mechanism that is potentially applicable to other voltage-dependent cation channels.

A new mechanistic framework for considering the homeostatic control of neuronal firing rates is presented.

As in humans, Drosophila hearts are able to maintain contractile performance during healthy aging, but this maintenance is associated with an increased susceptibility to progressive dysrhythmias that can lead to fibrillatory arrest.

Calmodulin mediates in the protective augmentation of K_V7-currents in response to oxidative stress in a calcium-dependent manner by an unconventional signaling mechanism.

The functional interaction of Na⁺ and K_ATP channels at the intercalated disk of cardiomyocytes depends on Ankyrin G and is clinically relevant since K_ATP channel mutations affect Na⁺ channel expression.