A Ca2+-based computational model for NDMA receptor-dependent synaptic plasticity at individual post-synaptic spines in the hippocampus
Associative synaptic plasticity is synapse specific and requires coincident activity in presynaptic and postsynaptic neurons to activate NMDA receptors (NMDARs). The resultant Ca2+ influx is the critical trigger for the induction of synaptic plasticity. Given its centrality for the induction of sy...
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| Format: | Article |
| Language: | English |
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Frontiers Media S.A.
2010-07-01
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| Series: | Frontiers in Synaptic Neuroscience |
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| Online Access: | http://journal.frontiersin.org/Journal/10.3389/fnsyn.2010.00031/full |
| _version_ | 1828777420536152064 |
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| author | Owen Rackham Krasimira Tsaneva-Atanasova Ayalvadi Ganesh Jack Mellor |
| author_facet | Owen Rackham Krasimira Tsaneva-Atanasova Ayalvadi Ganesh Jack Mellor |
| author_sort | Owen Rackham |
| collection | DOAJ |
| description | Associative synaptic plasticity is synapse specific and requires coincident activity in presynaptic and postsynaptic neurons to activate NMDA receptors (NMDARs). The resultant Ca2+ influx is the critical trigger for the induction of synaptic plasticity. Given its centrality for the induction of synaptic plasticity, a model for NMDAR activation incorporating the timing of presynaptic glutamate release and postsynaptic depolarization by back-propagating action potentials could potentially predict the pre- and post-synaptic spike patterns required to induce synaptic plasticity. We have developed such a model by incorporating currently available data on the timecourse and amplitude of the postsynaptic membrane potential within individual spines. We couple this with data on the kinetics of synaptic NMDARs and then use the model to predict the continuous spine [Ca2+] in response to regular or irregular pre- and post-synaptic spike patterns. We then incorporate experimental data from synaptic plasticity induction protocols by regular activity patterns to couple the predicted local peak [Ca2+] to changes in synaptic strength. We find that our model accurately describes [Ca2+] in dendritic spines resulting from NMDAR activation during presynaptic and postsynaptic activity when compared to previous experimental observations. The model also replicates the experimentally determined plasticity outcome of regular and irregular spike patterns when applied to a single synapse. This model could therefore be used to predict the induction of synaptic plasticity under a variety of experimental conditions and spike patterns. |
| first_indexed | 2024-12-11T16:20:13Z |
| format | Article |
| id | doaj.art-3f564ff2891b41c2893a19fa5eb75ff5 |
| institution | Directory Open Access Journal |
| issn | 1663-3563 |
| language | English |
| last_indexed | 2024-12-11T16:20:13Z |
| publishDate | 2010-07-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Synaptic Neuroscience |
| spelling | doaj.art-3f564ff2891b41c2893a19fa5eb75ff52022-12-22T00:58:51ZengFrontiers Media S.A.Frontiers in Synaptic Neuroscience1663-35632010-07-01210.3389/fnsyn.2010.000311356A Ca2+-based computational model for NDMA receptor-dependent synaptic plasticity at individual post-synaptic spines in the hippocampusOwen Rackham0Krasimira Tsaneva-Atanasova1Ayalvadi Ganesh2Jack Mellor3Bristol Centre for Complexity Sciences,School of Medical Science,University of BristolBristol Centre for Applied Non Linear Mathematics,School of Medical Science,University of BristolBristol Centre for Complexity Sciences,School of Medical Science,University of BristolUniversity of BristolAssociative synaptic plasticity is synapse specific and requires coincident activity in presynaptic and postsynaptic neurons to activate NMDA receptors (NMDARs). The resultant Ca2+ influx is the critical trigger for the induction of synaptic plasticity. Given its centrality for the induction of synaptic plasticity, a model for NMDAR activation incorporating the timing of presynaptic glutamate release and postsynaptic depolarization by back-propagating action potentials could potentially predict the pre- and post-synaptic spike patterns required to induce synaptic plasticity. We have developed such a model by incorporating currently available data on the timecourse and amplitude of the postsynaptic membrane potential within individual spines. We couple this with data on the kinetics of synaptic NMDARs and then use the model to predict the continuous spine [Ca2+] in response to regular or irregular pre- and post-synaptic spike patterns. We then incorporate experimental data from synaptic plasticity induction protocols by regular activity patterns to couple the predicted local peak [Ca2+] to changes in synaptic strength. We find that our model accurately describes [Ca2+] in dendritic spines resulting from NMDAR activation during presynaptic and postsynaptic activity when compared to previous experimental observations. The model also replicates the experimentally determined plasticity outcome of regular and irregular spike patterns when applied to a single synapse. This model could therefore be used to predict the induction of synaptic plasticity under a variety of experimental conditions and spike patterns.http://journal.frontiersin.org/Journal/10.3389/fnsyn.2010.00031/fullDendritic SpinesHippocampussynaptic plasticityNMDA receptorSpike timing-dependent plasticity |
| spellingShingle | Owen Rackham Krasimira Tsaneva-Atanasova Ayalvadi Ganesh Jack Mellor A Ca2+-based computational model for NDMA receptor-dependent synaptic plasticity at individual post-synaptic spines in the hippocampus Frontiers in Synaptic Neuroscience Dendritic Spines Hippocampus synaptic plasticity NMDA receptor Spike timing-dependent plasticity |
| title | A Ca2+-based computational model for NDMA receptor-dependent synaptic plasticity at individual post-synaptic spines in the hippocampus |
| title_full | A Ca2+-based computational model for NDMA receptor-dependent synaptic plasticity at individual post-synaptic spines in the hippocampus |
| title_fullStr | A Ca2+-based computational model for NDMA receptor-dependent synaptic plasticity at individual post-synaptic spines in the hippocampus |
| title_full_unstemmed | A Ca2+-based computational model for NDMA receptor-dependent synaptic plasticity at individual post-synaptic spines in the hippocampus |
| title_short | A Ca2+-based computational model for NDMA receptor-dependent synaptic plasticity at individual post-synaptic spines in the hippocampus |
| title_sort | ca2 based computational model for ndma receptor dependent synaptic plasticity at individual post synaptic spines in the hippocampus |
| topic | Dendritic Spines Hippocampus synaptic plasticity NMDA receptor Spike timing-dependent plasticity |
| url | http://journal.frontiersin.org/Journal/10.3389/fnsyn.2010.00031/full |
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