Calcium-based plasticity model explains sensitivity of synaptic changes to spike pattern, rate, and dendritic location.
dc.contributor.author | Graupner, Michael | |
dc.contributor.author | Brunel, Nicolas | |
dc.date.accessioned | 2021-06-06T16:29:14Z | |
dc.date.available | 2021-06-06T16:29:14Z | |
dc.date.issued | 2012-03 | |
dc.date.updated | 2021-06-06T16:29:09Z | |
dc.description.abstract | Multiple stimulation protocols have been found to be effective in changing synaptic efficacy by inducing long-term potentiation or depression. In many of those protocols, increases in postsynaptic calcium concentration have been shown to play a crucial role. However, it is still unclear whether and how the dynamics of the postsynaptic calcium alone determine the outcome of synaptic plasticity. Here, we propose a calcium-based model of a synapse in which potentiation and depression are activated above calcium thresholds. We show that this model gives rise to a large diversity of spike timing-dependent plasticity curves, most of which have been observed experimentally in different systems. It accounts quantitatively for plasticity outcomes evoked by protocols involving patterns with variable spike timing and firing rate in hippocampus and neocortex. Furthermore, it allows us to predict that differences in plasticity outcomes in different studies are due to differences in parameters defining the calcium dynamics. The model provides a mechanistic understanding of how various stimulation protocols provoke specific synaptic changes through the dynamics of calcium concentration and thresholds implementing in simplified fashion protein signaling cascades, leading to long-term potentiation and long-term depression. The combination of biophysical realism and analytical tractability makes it the ideal candidate to study plasticity at the synapse, neuron, and network levels. | |
dc.identifier | 1109359109 | |
dc.identifier.issn | 0027-8424 | |
dc.identifier.issn | 1091-6490 | |
dc.identifier.uri | ||
dc.language | eng | |
dc.publisher | Proceedings of the National Academy of Sciences | |
dc.relation.ispartof | Proceedings of the National Academy of Sciences of the United States of America | |
dc.relation.isversionof | 10.1073/pnas.1109359109 | |
dc.subject | Hippocampus | |
dc.subject | Neocortex | |
dc.subject | Dendrites | |
dc.subject | Synapses | |
dc.subject | Humans | |
dc.subject | Calcium | |
dc.subject | Models, Statistical | |
dc.subject | Calcium Signaling | |
dc.subject | Synaptic Transmission | |
dc.subject | Neuronal Plasticity | |
dc.subject | Long-Term Potentiation | |
dc.subject | Models, Biological | |
dc.subject | Computer Simulation | |
dc.subject | Long-Term Synaptic Depression | |
dc.title | Calcium-based plasticity model explains sensitivity of synaptic changes to spike pattern, rate, and dendritic location. | |
dc.type | Journal article | |
pubs.begin-page | 3991 | |
pubs.end-page | 3996 | |
pubs.issue | 10 | |
pubs.organisational-group | School of Medicine | |
pubs.organisational-group | Physics | |
pubs.organisational-group | Neurobiology | |
pubs.organisational-group | Duke Institute for Brain Sciences | |
pubs.organisational-group | Center for Cognitive Neuroscience | |
pubs.organisational-group | Duke | |
pubs.organisational-group | Trinity College of Arts & Sciences | |
pubs.organisational-group | Basic Science Departments | |
pubs.organisational-group | University Institutes and Centers | |
pubs.organisational-group | Institutes and Provost's Academic Units | |
pubs.publication-status | Published | |
pubs.volume | 109 |