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Journal of Experimental Biology, Vol 153, Issue 1 177-197, Copyright © 1990 by Company of Biologists
JOURNAL ARTICLES |
W Singer
Max-Planck-Institute for Brain Research, Frankfurt am Main, FRG.
During a critical period of postnatal development of the mammalian visual cortex, synaptic connections are susceptible to use-dependent modifications. Synaptic connections strengthen if pre- and postsynaptic elements are active simultaneously and postsynaptic depolarization is sufficient to allow for the activation of N-methyl-D-aspartate (NMDA)-receptor-gated conductances. By contrast, synaptic gain decreases if postsynaptic activation exceeds a critical threshold and presynaptic afferents are not capable of activating NMDA-receptor-dependent conductances. These processes lead to selective stabilization of connections between neuronal elements which often exhibit correlated activity and thus modify connectivity according to functional criteria. It is suggested that such experience-dependent selection of circuits serves different purposes at different levels of visual processing. At the input stage to the striate cortex it contributes to optimize the match between the representations of the two eyes. At a later stage of processing it participates in the development of selective connections between cortical columns and thereby serves to establish neuronal representations for frequently occurring constellations of features. Use-dependent changes of synaptic gain can also be induced in the mature visual cortex. These modifications follow the same rules as those occurring during early development and appear to depend on similar molecular mechanisms. However, in the adult the changes of synaptic gain do not seem to be followed by major rearrangements of connectivity. This suggests developmental alterations in mechanisms responsible for growth, removal and stabilization of synaptic connections. Actually, many of the cellular mechanisms thought to be involved in use-dependent synaptic plasticity change during development but it is still unclear which of them are responsible for the definitive stabilization of functionally confirmed pathways.
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