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Electrophysiology, optogenetics, and imaging in a mouse model of Dravet syndrome reveals dentate gyrus circuit dysfunction driven by hyperexcitability of the perforant path input from entorhinal cortex that can be modulated by recruitment of parvalbumin-expressing inhibitory interneurons.

Glutamate cotransmission from a subset of cortical GABAergic interneurons can promote network hyperexcitability.

Anoctamin/TMEM16 and SLC12 co-transporter genes selectively function in regulating cold nociception via excitatory chloride currents and can promote neuropathic sensitization phenotypes, including behavioral sensitization and neuronal hyperexcitability in Drosophila multimodal sensory neurons.

Aging reduces the potassium M current in sympathetic motor neurons, resulting in a hyperactive phenotype that can be reversed by pharmacological activation of these channels.

Mice that successfully avoid developing tinnitus despite exposure to excessive noise show spontaneous recovery of KCNQ2/3 potassium channel activity associated with a reduction in HCN channel activity in auditory brainstem neurons.

A powerful new fluorescence approach elucidates the structural mechanism for a specialized ion channel behavior important for cardiac and neuronal excitability.

Astrocytes modulate synaptic remodeling of developing circuits in a cell type-specific manner, with long lasting deficits in synaptic plasticity.

The expression and function of the cation channel TRPM3 is strongly increased in sensory neurons innervating inflamed tissue, likely contributing to inflammatory hyperalgesia and persistent pain.

An inducedpluripotent stem cell (iPSC)-based model of KCNQ2-associated developmental epileptic encephalopathy suggests that disease is driven by dyshomeostaic neuronal mechanisms that are downstream of loss of M-current.

Single-cell RNA-sequencing unraveled cell subtype-specific transcriptomic changes in both injured and uninjured primary sensory neurons after nerve injury and demonstrated transcriptomic sexual dimorphism.