Activity-Dependent Plasticity of the NMDA-Receptor Fractional Ca(2+) Current. Export

@article{citeulike:1024756, abstract = {Ca(2+) influx through NMDA receptors (NMDA-Rs) triggers synaptic plasticity, gene transcription, and cytotoxicity, but little is known about the regulation of NMDA-Rs themselves. We used two-photon glutamate uncaging to activate NMDA-Rs on individual dendritic spines in rat CA1 neurons while we measured NMDA-R currents at the soma and [Ca(2+)] changes in spines. Low-frequency uncaging trains induced Ca(2+)-dependent long-term depression of NMDA-R-mediated synaptic currents. Additionally, uncaging trains caused a reduction in the Ca(2+) accumulation per unit of NMDA-R current in spines due to a reduction in the fraction of the NMDA-R current carried by Ca(2+). Induction of depression of NMDA-R-mediated Ca(2+) influx required activation of NR2B-containing receptors. Receptors in single spines depressed rapidly in an all-or-none manner. These adaptive changes in NMDA-R function likely play a critical role in metaplasticity and in stabilizing activity levels in neuronal networks with Hebbian synapses.}, address = {Howard Hughes Medical Institute, Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724, USA.}, author = {Sobczyk, A. and Svoboda, K.}, citeulike-article-id = {1024756}, citeulike-linkout-0 = {http://dx.doi.org/10.1016/j.neuron.2006.11.016}, citeulike-linkout-1 = {http://view.ncbi.nlm.nih.gov/pubmed/17196527}, citeulike-linkout-2 = {http://www.hubmed.org/display.cgi?uids=17196527}, citeulike-linkout-3 = {http://www.sciencedirect.com/science/article/B6WSS-4MR8D3D-5/2/56ad5dfc66dcda886873cfbf7967a927}, day = {4}, doi = {10.1016/j.neuron.2006.11.016}, issn = {0896-6273}, journal = {Neuron}, keywords = {calcium, hippocampus, mni-glutamate, nmda-receptor, two-photon, uncaging}, month = {January}, number = {1}, pages = {17--24}, posted-at = {2007-01-04 11:51:02}, priority = {3}, title = {Activity-Dependent Plasticity of the NMDA-Receptor Fractional Ca(2+) Current.}, url = {http://dx.doi.org/10.1016/j.neuron.2006.11.016}, volume = {53}, year = {2007} }

TY - JOUR ID - citeulike:1024756 L3 - citeulike-article-id:1024756 N2 - Ca(2+) influx through NMDA receptors (NMDA-Rs) triggers synaptic plasticity, gene transcription, and cytotoxicity, but little is known about the regulation of NMDA-Rs themselves. We used two-photon glutamate uncaging to activate NMDA-Rs on individual dendritic spines in rat CA1 neurons while we measured NMDA-R currents at the soma and [Ca(2+)] changes in spines. Low-frequency uncaging trains induced Ca(2+)-dependent long-term depression of NMDA-R-mediated synaptic currents. Additionally, uncaging trains caused a reduction in the Ca(2+) accumulation per unit of NMDA-R current in spines due to a reduction in the fraction of the NMDA-R current carried by Ca(2+). Induction of depression of NMDA-R-mediated Ca(2+) influx required activation of NR2B-containing receptors. Receptors in single spines depressed rapidly in an all-or-none manner. These adaptive changes in NMDA-R function likely play a critical role in metaplasticity and in stabilizing activity levels in neuronal networks with Hebbian synapses. IS - 1 JF - Neuron SN - 0896-6273 AD - Howard Hughes Medical Institute, Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724, USA. EP - 24 TI - Activity-Dependent Plasticity of the NMDA-Receptor Fractional Ca(2+) Current. VL - 53 SP - 17 KW - calcium KW - hippocampus KW - mni-glutamate KW - nmda-receptor KW - two-photon KW - uncaging AU - Sobczyk, A AU - Svoboda, K PY - 2007/01/04/ UR - http://dx.doi.org/10.1016/j.neuron.2006.11.016 ER -