The development of the mammalian visual system begins prenatally at distributed sites, where cells generated at different embryonic ages are destined to interconnect and form the visual pathways, and ends postnatally with the functional tuning of neuronal receptive-field properties. It is reasonable to assume that the earliest stages in this developmental sequence are completed prior to the onset of neural activity, and also that activity may play only a minor role or even none at all in primary axon outgrowth and pathway finding (Harris, 1981; Harris and Holt, 1990). However, recent evidence indicates that subsequent events in development, such as the sorting of axons at their targets, the cellular differentiation of target cells and the formation of synaptic contacts by developing axons, are all influenced by action potentials. Action potentials in the developing retino-geniculo-cortical pathway can be eliminated by blocking the voltage-gated sodium channel with tetrodotoxin. Prenatal blockade prevents the laminar segregation of retinogeniculate axons. Postnatal blockade interrupts the formation of retinogeniculate synaptogenesis, slows the cytoarchitectonic differentiation of the lateral geniculate nucleus and produces abnormalities in the responses of lateral geniculate neurons. In the visual cortex, the development of cells and synapses is retarded and the eye-specific separation of geniculocortical axons is halted, thereby blocking the formation of ocular dominance columns. While the cellular mechanisms underlying these effects are not understood, a partial restoration of normal development can be produced by stimulating blocked axonal pathways electrically.

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