Journal
NEURON
Volume 28, Issue 1, Pages 245-259Publisher
CELL PRESS
DOI: 10.1016/S0896-6273(00)00100-8
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Funding
- NINDS NIH HHS [R01 NS037731-03, R01 NS037731-02, R01 NS037731-01A1, R01 NS037731-02S1, NS37731, NS34659, R01 NS037731-04, NS20147, R01 NS037731] Funding Source: Medline
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It is an open question whether new synapses form during hippocampal LTP. Here, we show that late-phase LTP (L-LTP) is associated with a significant increase in numbers of synaptic puncta identified by synaptophysin and N-cadherin, an adhesion protein involved in synapse formation during development. During potentiation, protein levels of N-cadherin are significantly elevated and N-cadherin dimerization is enhanced. The increases in synaptic number and N-cadherin levels are dependent on cAMP-dependent protein kinase (PKA) and protein synthesis, both of which are also required for L-LTP. Blocking N-cadherin adhesion prevents the induction of L-LTP, but not the early-phase of LTP (E-LTP). Our data suggest that N-cadherin is synthesized during the induction of L-LTP and recruited to newly forming synapses. N-cadherin may play a critical role in L-LTP by hording nascent pre- and postsynaptic membranes in apposition, enabling incipient synapses to acquire function and contribute to potentiation.
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