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Calcium base plasticity rule can predict plasticity direction for a variety of stimulation paradigms
Abstract   Open access   Peer reviewed

Calcium base plasticity rule can predict plasticity direction for a variety of stimulation paradigms

Joanna Jedrzejewska-Szmek, Daniel B Dorman and Kim T Blackwell
BMC neuroscience, Vol.18, 59 P15
26th Annual Computational Neuroscience Meeting (University of Antwerp Antwerp, Belgium, 07/15/2017–07/20/2017)
2017
url
https://doi.org/10.1186/s12868-017-0371-2View
Open Access

Abstract

The striatum is a major site of learning and memory formation for both sequence learning and habit formation. Synaptic plasticity – the long-lasting, activity dependent change in synaptic strength – is one of the mechanisms utilized by the brain for memory storage. Elevation in intracellular calcium is required in all forms of synaptic plasticity. It is widely believed that the amplitude and duration of calcium transients can determine direction of plasticity. It is not certain, however, if this hypothesis can be utilized in the striatum, partly because dopamine is required in potentiation of synaptic responses and partly because the diversity in stimulation paradigms is likely to produce a wide variety of calcium concentrations. To evaluate whether the direction of synaptic plasticity in the striatum can be predicted based on calcium dynamics, we used a model spiny projection neuron (SPN) and a calcium-based plasticity-rule. The SPN model utilized sophisticated calcium dynamics, which included calcium diffusion, buffering and pump extrusion both in the dendritic tree and spines, and also included synaptic AMPAR desensitization to more accurately model frequency dependent plasticity paradigms. The calcium based plasticity rule has been successfully used before [1] to predict plasticity direction of three spike-timing dependent plasticity (STDP) induction paradigms. To further test the rule, we utilized two frequency-dependent plasticity paradigms, one that elicits long-term depression (LTD) and one that elicits long-term potentiation (LTP). Our simulations show that, despite the variation in calcium for different protocols, a single, calcium-based weight change rule (plasticity rule) can explain the change in synaptic weights for two frequency dependent plasticity paradigms. Furthermore, using calcium-based weight change rule we tested whether excitability and possible changes in dopamine depletion on excitability of direct (dSPN) and indirect pathway spiny projection neurons (iSPN) can account for different outcome of STDP paradigm presented in [2] and [3]. Elucidating the mechanisms underlying synaptic plasticity, especially the role and interplay of calcium and dopamine, will allow for better understanding mechanisms of memory storage in health and disease.

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