Searching across hundreds of databases

Our searching services are busy right now. Your search will reload in five seconds.

X
Forgot Password

If you have forgotten your password you can enter your email here and get a temporary password sent to your email.

The effects of NMDA subunit composition on calcium influx and spike timing-dependent plasticity in striatal medium spiny neurons.

Calcium through NMDA receptors (NMDARs) is necessary for the long-term potentiation (LTP) of synaptic strength; however, NMDARs differ in several properties that can influence the amount of calcium influx into the spine. These properties, such as sensitivity to magnesium block and conductance decay kinetics, change the receptor's response to spike timing dependent plasticity (STDP) protocols, and thereby shape synaptic integration and information processing. This study investigates the role of GluN2 subunit differences on spine calcium concentration during several STDP protocols in a model of a striatal medium spiny projection neuron (MSPN). The multi-compartment, multi-channel model exhibits firing frequency, spike width, and latency to first spike similar to current clamp data from mouse dorsal striatum MSPN. We find that NMDAR-mediated calcium is dependent on GluN2 subunit type, action potential timing, duration of somatic depolarization, and number of action potentials. Furthermore, the model demonstrates that in MSPNs, GluN2A and GluN2B control which STDP intervals allow for substantial calcium elevation in spines. The model predicts that blocking GluN2B subunits would modulate the range of intervals that cause long term potentiation. We confirmed this prediction experimentally, demonstrating that blocking GluN2B in the striatum, narrows the range of STDP intervals that cause long term potentiation. This ability of the GluN2 subunit to modulate the shape of the STDP curve could underlie the role that GluN2 subunits play in learning and development.

Pubmed ID: 22536151 RIS Download

Mesh terms: Action Potentials | Animals | Calcium | Computer Simulation | Corpus Striatum | Humans | Models, Chemical | Models, Neurological | N-Methylaspartate | Neuronal Plasticity | Neurons | Protein Subunits | Structure-Activity Relationship

Publication data is provided by the National Library of Medicine ® and PubMed ®. Data is retrieved from PubMed ® on a weekly schedule. For terms and conditions see the National Library of Medicine Terms and Conditions.

This is a list of tools and resources that we have found mentioned in this publication.


ModelDB

A curated database of published models in the broad domain of computational neuroscience. ModelDB provides an accessible location for storing and efficiently retrieving computational neuroscience models. ModelDB is tightly coupled with NeuronDB. Models can be coded in any language for any environment. Model code can be viewed before downloading and browsers can be set to auto-launch the models. ModelDB addresses the need for access to such models in order to evaluate their validity and extend their use. It can handle computational models expressed in any textual form, including procedural or declarative languages (e.g. C , XML dialects) and source code written for any simulation environment. The model source code doesn't even have to reside inside ModelDB; it just has to be available from some publicly accessible online repository or WWW site. ModelDB is curated in order to maximize the scientific utility of its contents. The ideal model entry would contain original (author-written) source code, especially if it works and reproduces at least one figure from a published article. Original source code has tremendous value because it is what the authors used to generate the simulation results from which they derived their published insights and conclusions. High quality third party re-implementations of published models are also relevant, especially those involving models that are of wide interest.

tool

View all literature mentions