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Inhibition of bAPs and Ca2+ spikes in a multi-compartment pyramidal neuron model (Wilmes et al 2016)
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"Synaptic plasticity is thought to induce memory traces in the brain that are the foundation of learning. To ensure the stability of these traces in the presence of further learning, however, a regulation of plasticity appears beneficial. Here, we take up the recent suggestion that dendritic inhibition can switch plasticity of excitatory synapses on and off by gating backpropagating action potentials (bAPs) and calcium spikes, i.e., by gating the coincidence signals required for Hebbian forms of plasticity. We analyze temporal and spatial constraints of such a gating and investigate whether it is possible to suppress bAPs without a simultaneous annihilation of the forward-directed information flow via excitatory postsynaptic potentials (EPSPs). In a computational analysis of conductance-based multi-compartmental models, we demonstrate that a robust control of bAPs and calcium spikes is possible in an all-or-none manner, enabling a binary switch of coincidence signals and plasticity. ..."
Wilmes KA, Sprekeler H, Schreiber S (2016) Inhibition as a Binary Switch for Excitatory Plasticity in Pyramidal Neurons.
PLoS Comput Biol
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Neuron or other electrically excitable cell;
Hippocampus CA1 pyramidal GLU cell;
Neocortex V1 L6 pyramidal corticothalamic GLU cell;
Dendritic Action Potentials;
Wilmes, Katharina A. [katharina.wilmes at googlemail.com];
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Hippocampus CA1 pyramidal GLU cell
Neocortex V1 L6 pyramidal corticothalamic GLU cell
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