2024-03-28T19:34:16Zhttp://digital.csic.es/dspace-oai/requestoai:digital.csic.es:10261/617562021-12-27T16:41:44Zcom_10261_54com_10261_1col_10261_307
The muscarinic long-term enhancement of NMDA and AMPA receptor-mediated transmission at Schaffer collateral synapses develop through different intracellular mechanisms
Fernández de Sevilla, D.
Buño, Washington
We had described a muscarinic-mediated long-term synaptic enhancement at Schaffer collateral synapses caused by the insertion of AMPARs in spines of rat hippocampal CA1 pyramidal neurons that requires Ca2+ release from IP3-sensitive stores (Fernández de Sevilla et al., 2008). We now show that this AMPA-mediated LTPIP3 is precisely matched by an amplification of NMDAR-mediated transmission. The enhanced AMPAR transmission involves SNARE protein activity and CaMKII activation. The amplification of NMDA transmission requires combined CaMKII, PKC, and SRC kinase activity without detectable surface incorporation of NMDARs, suggesting that changes in receptor properties mediate this process. The enhanced AMPAR- and NMDAR-mediated transmission markedly reduce the induction threshold of >Hebbian> LTP. We conclude that both modes of glutamatergic synaptic potentiation may play a critical functional role in the regulation of the learning machinery of the brain by adding flexibility to the demands of the hippocampal network. Copyright © 2010 the authors.
Peer Reviewed
2012-12-03T12:25:06Z
2012-12-03T12:25:06Z
2010
2012-12-03T12:25:06Z
artículo
http://purl.org/coar/resource_type/c_6501
doi: 10.1523/JNEUROSCI.1848-10.2010
issn: 0270-6474
Journal of Neuroscience 30: 11032- 11042 (2010)
http://hdl.handle.net/10261/61756
10.1523/JNEUROSCI.1848-10.2010
20720110
en
none
Society for Neuroscience