Neural activity plays roles in the later stages of development of cortical excitatory neurons, including dendritic and axonal arborization, remodeling, and synaptogenesis. However, its role in earlier stages, such as migration and dendritogenesis, is less clear. Here we investigated roles of neural activity in the maturation of cortical neurons, using calcium imaging and expression of prokaryotic voltage-gated sodium channel, NaChBac. Calcium imaging experiments showed that postmigratory neurons in layer II/III exhibited more frequent spontaneous calcium transients than migrating neurons. To test whether such an increase of neural activity may promote neuronal maturation, we elevated the activity of migrating neurons by NaChBac expression. Elevation of neural activity impeded migration, and induced premature branching of the leading process before neurons arrived at layer II/III. Many NaChBac-expressing neurons in deep cortical layers were not attached to radial glial fibers, suggesting that these neurons had stopped migration. Morphological and immunohistochemical analyses suggested that branched leading processes of NaChBac-expressing neurons differentiated into dendrites. Our results suggest that developmental control of spontaneous calcium transients is critical for maturation of cortical excitatory neurons in vivo: keeping cellular excitability low is important for migration, and increasing spontaneous neural activity may stop migration and promote dendrite formation.
The propagation of the change in membrane potential between two aqueous phases across two parallel membranes from the sending site to the receiving site was elucidated. The potential differences at every interface are controlled by the ion transfers and the circulating current flowed to keep the electroneutrality of every phase.
Propagation of a change in a potential difference between two aqueous phases (W1 and W2) across a membrane was examined by using three membrane cells (A, B and C). At first, the cell A was electrically connected with the cell B by controlling the ionic compositions. By changing the connection with the cell A from the cell B to the cell C indicating the different membrane potential, the change of the membrane potential was propagated. The delay and decrement of the propagation was observed by setting capacitors or resistors in the electric circuit.
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