Activity-dependent Plasticity of the Nmda-receptor Fractional Ca2+ Current.
From: Howard Hughes Medical Institute, Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724, USA.
Neuron
- Publish Date: Jan 2007
- ISSN: 0896-6273
- Volume: 53
- Issue: 1
- Pages: 17-24
- Medium: Print
- Language: English
- Citation (JAMA): Sobczyk Aleksander, Svoboda Karel, et al. Activity-dependent Plasticity of the Nmda-receptor Fractional Ca2+ Current.. Neuron Jan 2007;53:17-24
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.
Mesh Headings (Keywords): Animals, Calcium, Calcium Signaling, Dendritic Spines, Glutamic Acid, Hippocampus, Long-Term Synaptic Depression, Nerve Net, Neural Pathways, Neuronal Plasticity, Organ Culture Techniques, Patch-Clamp Techniques, Pyramidal Cells, Rats, Rats, Sprague-Dawley, Receptors, N-Methyl-D-Aspartate, Synaptic Transmission
Check for Full Text / PubMed Unique Identifier (PMID): 17196527
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