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Computational models are helping researchers to understand how certain properties of neurons contribute to respiratory rhythms.

The voltage-gated sodium channel Na_v1.1 is identified as an essential component of the proprioceptive transmission machinery that is required in vivo for normal motor behavior.

Computational modeling reveals the mechanisms by which a diverse group of neurons in the brainstem generates rhythmic breathing in mammals.

The membrane nonlinearities of the dendritic arbor of striatal cholinergic interneurons conspire with the spatial distribution of its excitatory inputs to preferentially boost thalamic inputs.

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.

External calcium regulates neuronal excitability via its actions on voltage-gated sodium channels but not by regulating NALCN via the calcium-sensing receptor.

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.

A-type potassium conductances influence the distinctive firing behaviour of irregular-spiking interneurons.

Variants in FGF13, associated with developmental and epileptic encephalopathies, alter neuronal excitability by affecting inhibitory neurons and by a sodium channel-independent mechanism.

Mathematical models with experimental validation show that chloride transporters in the cell membrane, and not negatively charged impermeant molecules, generate the driving force used by GABA receptors to silence neurons.