The mammalian neocortex consists of columnar circuits, whose development may be controlled by patterns of spontaneous activity. Columnar domains of spontaneously coactive neurons were previously described using Ca2+ imaging of slices from developing rat neocortex. We have now investigated the cellular mechanisms responsible for the coactivation of these domains. The activation starts in the center of a domain and spreads at speeds of approximately 100 microns/s. Domains occur in the presence of tetrodotoxin but are blocked by the gap junction blockers halothane and octanol. Simultaneous intracellular and optical recordings from dye-coupled cells reveal functional coupling between developing neocortical neurons. These data support the hypothesis that a neuronal domain results from the spontaneous excitation of one or a few trigger neurons that subsequently activate, either electrically or biochemically, the rest of the cells via gap junctions.
Cone arrestin can partially substitute for rod arrestin in arr1-/- rods, offering a degree of protection from light-induced damage and increasing the extent of rhodopsin deactivation in response to flashes of light. Although earlier work has shown that rod arrestin can bind and deactivate cone pigments efficiently, the results suggest that cone arrestin binds light-activated, phosphorylated rhodopsin less efficiently than does rod arrestin in vivo. These results suggest that the structural requirements for high-affinity binding are fundamentally distinct for rod and cone arrestins.
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