E7 Synaptic plasticity (Hebb, LTP/LTD, STDP)

Topic

Synaptic plasticity describes how the effective weight of a synapse—proportional to the channel conductance defined for that synapse—changes based on the correlated activity between the presynaptic and postsynaptic neurons it connects.

The classical Hebbian rule posits that the effective synaptic weight increases when the presynaptic and postsynaptic neurons are simultaneously active. A variant of this rule, Oja's rule, introduces a normalization term to the effective synaptic weight; this prevents the weight from growing without bound even if correlated activity persists: the closer the effective synaptic weight is to its upper limit, the less it increases in response to the same correlated activity.

In contrast, the Bienstock-Cooper-Munro model introduces a sliding threshold for the effective synaptic weight that depends on the postsynaptic neuron's average activity: the higher the recent average postsynaptic activity, the higher this sliding threshold is set. Thanks to this sliding threshold, the same correlated activity between the presynaptic and postsynaptic neurons can lead to potentiation of the effective synaptic weight at one time and depression of that same weight at another, depending on the postsynaptic neuron's recent activity history.

Spike-timing-dependent plasticity further captures an experimentally observed causal asymmetry in the effective synaptic weight: when the presynaptic neuron fires before the postsynaptic neuron, the effective synaptic weight tends to be potentiated, whereas when the firing order is reversed, the weight tends to be depressed. In biophysical terms, all these changes in effective synaptic weight—whether described by Hebb's rule, Oja's rule, the Bienenstock-Cooper-Munro model, or spike-timing-dependent plasticity—are largely mediated by the intracellular calcium concentration in the postsynaptic neuron, which acts as a common signal; depending on the magnitude and temporal dynamics of this postsynaptic intracellular calcium, that common signal triggers a cascade leading to either long-term potentiation or long-term depression of the effective synaptic weight. Ultimately, it is this very effective synaptic weight—shaped by correlated activity between the presynaptic and postsynaptic neurons and mediated by postsynaptic intracellular calcium—that undergoes directed change in accordance with the various described rules of synaptic plasticity.

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