Tune it in: mechanisms and computational significance of neuron-autonomous plasticity.

Abstract

The activity of a neural network is a result of synaptic signals that convey the communication between neurons and neuron-based intrinsic currents that determine the neuron's input-output transfer function. Ample studies have demonstrated that cell-based excitability, and in particular intrinsic excitability, is modulated by learning and that these modifications play a key role in learning-related behavioral changes. The field of cell-based plasticity is largely growing, and it entails numerous experimental findings that demonstrate a large diversity of currents that are affected by learning. The diverse effect of learning on the neuron's excitability emphasizes the need for a framework under which cell-based plasticity can be categorized to enable the assessment of the computational roles of the intrinsic modifications. We divide the domain of cell-based plasticity into three main categories, where the first category entails the currents that mediate the passive properties and single-spike generation, the second category entails the currents that mediate spike frequency adaptation, and the third category entails a novel learning-induced mechanism where all excitatory and inhibitory synapses double their strength. Curiously, this elementary division enables a natural categorization of the computational roles of these learning-induced plasticities. The computational roles are diverse and include modification of the neuronal mode of action, such as bursting, prolonged, and fast responsive; attention-like effect where the signal detection is improved; transfer of the network into an active state; biasing the competition for memory allocation; and transforming an environmental cue into a dominant cue and enabling a quicker formation of new memories.