Abstract
Homosynaptic Hebbian-type plasticity provides a cellular mechanism of learning and refinement of connectivity during development in a variety of biological systems. In this review we argue that a complimentary form of plasticity—heterosynaptic plasticity—represents a necessary cellular component for homeostatic regulation of synaptic weights and neuronal activity. The required properties of a homeostatic mechanism which acutely constrains the runaway dynamics imposed by Hebbian associative plasticity have been well-articulated by theoretical and modeling studies. Such mechanism(s) should robustly support the stability of operation of neuronal networks and synaptic competition, include changes at non-active synapses, and operate on a similar time scale to Hebbian-type plasticity. The experimentally observed properties of heterosynaptic plasticity have introduced it as a strong candidate to fulfill this homeostatic role. Subsequent modeling studies which incorporate heterosynaptic plasticity into model neurons with Hebbian synapses (utilizing an STDP learning rule) have confirmed its ability to robustly provide stability and competition. In contrast, properties of homeostatic synaptic scaling, which is triggered by extreme and long lasting (hours and days) changes of neuronal activity, do not fit two crucial requirements for a hypothetical homeostatic mechanism needed to provide stability of operation in the face of on-going synaptic changes driven by Hebbian-type learning rules. Both the trigger and the time scale of homeostatic synaptic scaling are fundamentally different from those of the Hebbian-type plasticity. We conclude that heterosynaptic plasticity, which is triggered by the same episodes of strong postsynaptic activity and operates on the same time scale as Hebbian-type associative plasticity, is ideally suited to serve a homeostatic role during on-going synaptic plasticity.
Highlights
Three Forms of Synaptic PlasticityNormal operation of the brain requires the maintenance of balances across various neuronal and synaptic features, and keeping key factors within their operating ranges
The required properties of a homeostatic mechanism which acutely constrains the runaway dynamics imposed by Hebbian associative plasticity have been well-articulated by theoretical and modeling studies
The experimentally observed properties of heterosynaptic plasticity have introduced it as a strong candidate to fulfill this homeostatic role
Summary
Normal operation of the brain requires the maintenance of balances across various neuronal and synaptic features, and keeping key factors within their operating ranges. It occurs only at synapses that were directly involved in activation of a cell during the induction, for example during afferent tetanization or pairing procedure (Figure 1A) This form of plasticity is called input specific, and, if the induction follows Hebbian-type learning rules, associative (Bliss and Collingridge, 1993). Hebbian-type learning rules impose an intrinsic positive feedback on synaptic weight changes, making the system prone to runaway dynamics of synaptic weights and activity They introduce only a weak degree of competition between synapses. Homosynaptic plasticity, while being a major driving force for synaptic changes mediating associative learning, imposes positive feedback on synaptic changes which creates energetically and computationally unstable runaway dynamics It does not provide the required degree of synaptic competition known to be necessary for many types of learning. It has not been clear, which of the multitude of proposed physiological mechanisms is/are able to serve these roles
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