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Friedrich Miescher Institute, CH-4002 Basel, Switzerland
Long-term functional plasticity in the nervous system can involve structural changes in terminal
arborization and synaptic connections. To determine
whether the differential expression of intrinsic neuronal determinants affects structural plasticity, we produced and analyzed transgenic mice overexpressing the
cytosolic proteins cortical cytoskeleton-associated protein 23 (CAP-23) and growth-associated protein 43 (GAP-43) in adult neurons.
Like GAP-43, CAP-23 was downregulated in mouse
motor nerves and neuromuscular junctions during the
second postnatal week and reexpressed during regeneration. In transgenic mice, the expression of either protein in adult motoneurons induced spontaneous and greatly potentiated stimulus-induced nerve sprouting at
the neuromuscular junction. This sprouting had transgene-specific features, with CAP-23 inducing longer,
but less numerous sprouts than GAP-43. Crossing of
the transgenic mice led to dramatic potentiation of the
sprout-inducing activities of GAP-43 and CAP-23, indicating that these related proteins have complementary
and synergistic activities. In addition to ultraterminal
sprouting, substantial growth of synaptic structures was
induced. Experiments with pre- and postsynaptic toxins
revealed that in the presence of GAP-43 or CAP-23,
sprouting was stimulated by a mechanism that responds to reduced transmitter release and may be independent
of postsynaptic activation.
These results demonstrate the importance of intrinsic
determinants in structural plasticity and provide an experimental approach to study its role in nervous system
function.
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