Impaired GABAergic and glutamatergic synaptic function and loss of interneurons in the amygdala, hippocampus, and cerebellum cause characteristic disease symptoms in a mouse model juvenile neuronal ceroid lipofuscinosis.
Optogenetic techniques, whereby light is used to activate neuronal cells, are quickly becoming widely used in neuroscience; but excessive exposure to light can actually silence certain types of neuronal cells.
Oligodendrocytes in white matter use Kir4.1 inwardly rectifying potassium channels to prevent extracellular potassium accumulation, enabling neurons to sustain repetitive firing and limiting the initiation of seizures.
In mouse models of Huntington's disease, striatal spiny projection neurons up-regulate dendritic potassium channels, which impairs their normal function, but a zinc finger gene therapy can reverse this deficit.
Vasoactive intestinal peptide-expressing GABAergic interneurons in cerebral cortex express the sodium channel subunit Nav1.1, and a defined subset of VIP interneurons are dysfunctional in a mouse model of Dravet syndrome.
Comprehensive gene profiling of the hypothalamic hypocretin neurons, high resolution imaging and behavioral assays have revealed the molecular signature of these versatile neurons and identified a potassium channel that is required for nighttime sleep.