Abstract
Synaptic modifications induced at one synapse are accompanied by hetero-synaptic changes at neighboring sites. In addition, it is suggested that the mechanism of spatial association of synaptic plasticity is based on intracellular calcium signaling that is mainly regulated by two types of receptors of endoplasmic reticulum calcium store: the ryanodine receptor (RyR) and the inositol triphosphate receptor (IP3R). However, it is not clear how these types of receptors regulate intracellular calcium flux and contribute to the outcome of calcium-dependent synaptic change. To understand the relation between the synaptic association and store-regulated calcium dynamics, we focused on the function of RyR calcium regulation and simulated its behavior by using a computational neuron model. As a result, we observed that RyR-regulated calcium release depended on spike timings of pre- and postsynaptic neurons. From the induction site of calcium release, the chain activation of RyRs occurred, and spike-like calcium increase propagated along the dendrite. For calcium signaling, the propagated calcium increase did not tend to attenuate; these characteristics came from an all-or-none behavior of RyR-sensitive calcium store. Considering the role of calcium dependent synaptic plasticity, the results suggest that RyR-regulated calcium propagation induces a similar change at the synapses. However, according to the dependence of RyR calcium regulation on the model parameters, whether the chain activation of RyRs occurred, sensitively depended on spatial expression of RyR and nominal fluctuation of calcium flux. Therefore, calcium regulation of RyR helps initiate rather than relay calcium propagation.
Highlights
Synaptic modification is essential for developing and maintaining functional neural circuits and depends on neuronal activity (Bliss and Collingridge 1993; Katz and Shatz 1996; Martin et al 2000)
Results of physiological studies focusing on the dependence of synaptic plasticity on temporal activity of neurons have demonstrated that synaptic efficacy can either be long-term potentiated (LTP) or depressed (LTD) depending on firing rate (Bliss and Lomo 1973; Sjöström et al 2001) and relative spike timing (STDP) (Markram et al 1997; Bi and Poo 1998) of pre- and postsynaptic neurons
The first process is ryanodine receptor (RyR)-mediated calcium release from the endoplasmic reticulum (ER) induced by spike-triggered calcium influx via NMDA receptors (NMDARs) and amplitude of mem-Vol
Summary
Synaptic modification is essential for developing and maintaining functional neural circuits and depends on neuronal activity (Bliss and Collingridge 1993; Katz and Shatz 1996; Martin et al 2000). The spatial synaptic plasticity association has been observed in a global area: for example, CA1 and CA3 of the hippocampus (Lynch et al 1977; Bradler and Barrionuevo 1989; Nishiyama et al 2000), cortex (Hirsch et al 1992), and amygdala (Royer and Paré 2003). This evidence implies that individual synapses are not independent, and the outcome of synaptic modification is partly determined by the association between synapses. The spatial aspect of synaptic plasticity provides the possibility to construct and stabilize selectivity of synaptic input that functionally activates neuronal circuits
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