Synaptic homeostasis and input selectivity follow from a calcium-dependent plasticity model
AUTOR(ES)
Yeung, Luk Chong
FONTE
National Academy of Sciences
RESUMO
Modifications in the strengths of synapses are thought to underlie memory, learning, and development of cortical circuits. Many cellular mechanisms of synaptic plasticity have been investigated in which differential elevations of postsynaptic calcium concentrations play a key role in determining the direction and magnitude of synaptic changes. We have previously described a model of plasticity that uses calcium currents mediated by N-methyl-d-aspartate receptors as the associative signal for Hebbian learning. However, this model is not completely stable. Here, we propose a mechanism of stabilization through homeostatic regulation of intracellular calcium levels. With this model, synapses are stable and exhibit properties such as those observed in metaplasticity and synaptic scaling. In addition, the model displays synaptic competition, allowing structures to emerge in the synaptic space that reflect the statistical properties of the inputs. Therefore, the combination of a fast calcium-dependent learning and a slow stabilization mechanism can account for both the formation of selective receptive fields and the maintenance of neural circuits in a state of equilibrium.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=522010Documentos Relacionados
- Neuronal synchronization without calcium-dependent synaptic transmission in the hypothalamus.
- Phorbol esters enhance synaptic transmission by a presynaptic, calcium-dependent mechanism in rat hippocampus.
- Autophosphorylation-Dependent Activation of a Calcium-Dependent Protein Kinase from Groundnut1
- A Calcium-Dependent but Calmodulin-Independent Protein Kinase from Soybean 1
- Calcium-Dependent Norepinephrine Release from Presynaptic Nerve Endings In Vitro