RESUMEN
Various forms of synaptic plasticity, including spike timing-dependent plasticity, can be accounted for by calcium-dependent models of synaptic plasticity. However, recent results in which synaptic plasticity is induced by multi-spike protocols cannot simply be accounted for by linear superposition of plasticity due to spike pairs or by existing calcium-dependent models. In this paper, we show that multi-spike protocols can be accounted for if, in addition to the dynamics of back-propagating action potentials, stochastic synaptic dynamics are taken into account. We show that a stochastic implementation can account for the data better than a deterministic implementation and is also more robust. Our results demonstrate that differences between experimental results obtained in hippocampus and visual cortex can be accounted for by the different synaptic and dendritic dynamics in these two systems.
Asunto(s)
Potenciales de Acción/fisiología , Dendritas/fisiología , Hipocampo/fisiología , Plasticidad Neuronal/fisiología , Transmisión Sináptica/fisiología , Corteza Visual/fisiología , Animales , Humanos , Vías Nerviosas/fisiología , Dinámicas no Lineales , Terminales Presinápticos/fisiología , Tiempo de Reacción/fisiología , Reproducibilidad de los Resultados , Procesos EstocásticosRESUMEN
The influx of calcium ions into the dendritic spines through the N-methyl-D-aspartate (NMDA) channels is believed to be the primary trigger for various forms of synaptic plasticity. In this paper, the authors calculate analytically the mean values of the calcium transients elicited by a spiking neuron undergoing a simple model of ionic currents and back-propagating action potentials. The relative variability of these transients, due to the stochastic nature of synaptic transmission, is further considered using a simple Markov model of NMDA receptors. One finds that both the mean value and the variability depend on the timing between presynaptic and postsynaptic action potentials. These results could have implications for the expected form of the synaptic-plasticity curve and can form a basis for a unified theory of spike-time-dependent, and rate-based plasticity.
Asunto(s)
Potenciales de Acción/fisiología , Señalización del Calcio/fisiología , Modelos Neurológicos , N-Metilaspartato/fisiología , Plasticidad Neuronal/fisiología , Neuronas/fisiología , Médula Espinal/fisiología , Transmisión Sináptica/fisiología , Calcio/metabolismo , Simulación por Computador , Activación del Canal Iónico/fisiología , Modelos Estadísticos , Procesos EstocásticosRESUMEN
Different mechanisms that could form the molecular basis for bi-directional synaptic plasticity have been identified experimentally and corresponding biophysical models can be constructed. However, such models are complex and therefore it is hard to deduce their consequences to compare them to existing abstract models of synaptic plasticity. In this paper we examine two such models: a phenomenological one inspired by the phenomena of AMPA receptor insertion, and a more complex biophysical model based on the phenomena of AMPA receptor phosphorylation. We show that under certain approximations both these models can be mapped on to an equivalent, calcium-dependent, differential equation. Intracellular calcium concentration varies locally in each postsynaptic compartment, thus the plasticity rule we extract is a single-synapse rule. We convert this single synapse plasticity equation to a multi-synapse rule by incorporating a model of the NMDA receptor. Finally we suggest a mathematical embodiment of metaplasticity, which is consistent with observations on NMDA receptor properties and dependence on cellular activity. These results, in combination with some of our previous results, produce converging evidence for the calcium control hypothesis including a dependence of synaptic plasticity on the level of intercellular calcium as well as on the temporal pattern of calcium transients.