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Calcium dynamics predict direction of synaptic plasticity in striatal spiny projection neurons
Author(s) -
JędrzejewskaSzmek Joanna,
Damodaran Sriraman,
Dorman Daniel B.,
Blackwell Kim T.
Publication year - 2017
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/ejn.13287
Subject(s) - synaptic plasticity , neuroscience , nonsynaptic plasticity , homosynaptic plasticity , long term potentiation , metaplasticity , synaptic augmentation , striatum , synaptic scaling , calcium , plasticity , spike timing dependent plasticity , post tetanic potentiation , medium spiny neuron , biology , chemistry , dopamine , physics , inhibitory postsynaptic potential , excitatory postsynaptic potential , receptor , biochemistry , organic chemistry , thermodynamics
The striatum is a major site of learning and memory formation for sensorimotor and cognitive association. One of the mechanisms used by the brain for memory storage is synaptic plasticity – the long‐lasting, activity‐dependent change in synaptic strength. All forms of synaptic plasticity require an elevation in intracellular calcium, and a common hypothesis is that the amplitude and duration of calcium transients can determine the direction of synaptic plasticity. The utility of this hypothesis in the striatum is unclear in part because dopamine is required for striatal plasticity and in part because of the diversity in stimulation protocols. To test whether calcium can predict plasticity direction, we developed a calcium‐based plasticity rule using a spiny projection neuron model with sophisticated calcium dynamics including calcium diffusion, buffering and pump extrusion. We utilized three spike timing‐dependent plasticity ( STDP ) induction protocols, in which postsynaptic potentials are paired with precisely timed action potentials and the timing of such pairing determines whether potentiation or depression will occur. Results show that despite the variation in calcium dynamics, a single, calcium‐based plasticity rule, which explicitly considers duration of calcium elevations, can explain the direction of synaptic weight change for all three STDP protocols. Additional simulations show that the plasticity rule correctly predicts the NMDA receptor dependence of long‐term potentiation and the L‐type channel dependence of long‐term depression. By utilizing realistic calcium dynamics, the model reveals mechanisms controlling synaptic plasticity direction, and shows that the dynamics of calcium, not just calcium amplitude, are crucial for synaptic plasticity.