Serotonin neurons in chronically isolated mice become less responsive to excitatory stimulation, but inhibiting a distinctive calcium-activated potassium channel can restore both neuronal activity and behavior.
The activation of small-conductance calcium-activated potassium channels in spines by action potentials regulates the induction of spike-timing dependent synaptic plasticity during low-frequency single action potential–EPSP pairing.
Supporting cells in the cochlea change their shape in response to purinergic receptor activation, which influences hair cell excitability by altering potassium redistribution in the extracellular space.
The mammalian potassium channel KCa3.1, which is important for T- and B-cell activation, is inhibited by cytoplasmic copper, mediated by a histidine residue (His358) that is phosphorylated to activate the channel.
The principal potassium ion channel in human sperm, Slo3, is primarily activated by calcium ions and controls the membrane potential of human sperm by intracellular calcium ion levels rather than intracellular pH.
The development of the electrical phenotype of neurons can be precisely quantified and dissected using a combination of multi-variate statistical analyses and a systematic electrophysiological characterization of electrical properties.
Computational modeling motivated by recent experiments clarifies biophysical mechanisms generating the rhythm and amplitude of breathing at the level of neurons and brain circuits in mammals.
