Heterosynaptic Plasticity

Synaptic plasticity refers to a chemical synapse's ability to undergo changes in strength. Synaptic plasticity is typically input-specific (i.e. homosynaptic plasticity), meaning that the activity in a particular neuron alters the efficacy of a synaptic connection between that neuron and its target. However, in the case of heterosynaptic plasticity, the activity of a particular neuron leads to input unspecific changes in the strength of synaptic connections from other unactivated neurons. A number of distinct forms of heterosynaptic plasticity have been found in a variety of brain regions and organisms. These different forms of heterosynaptic plasticity contribute to a variety of neural processes including associative learning, the development of neural circuits, and homeostasis of synaptic input.

Heterosynaptic plasticity may play an important homeostatic role in neural plasticity by normalizing or limiting the total change of synaptic input during ongoing Hebbian plasticity. Hebbian plasticity, an ubiquitous form of homosynaptic, associative plasticity, is believed to underlie learning and memory. Moreover, Hebbian plasticity is induced by and amplifies correlations in neural circuits which creates a positive feedback loop and renders neural circuits unstable. To avoid this instability Hebbian plasticity needs to be constrained, for instance by the conservation of the total amount of synaptic input. This role is believed to be fulfilled by a diversity of homeostatic mechanisms.

However, to effectively stabilize Hebbian plasticity, which can be induced in a matter of seconds to minutes, homeostatic plasticity has to react rapidly. This requirement, however, is not met by most forms of homeostatic plasticity, which typically act on timescales of hours, days or longer. This limitation does not seem to apply to heterosynaptic plasticity.

To achieve a homeostatic effect, heterosynaptic plasticity serving a homeostatic role have to cause pathway unspecific synaptic changes in the opposite direction as Hebbian plasticity. In other words, whenever homosynaptic long-term potentiation is induced at a given synapse, other unstimulated synapses should be depressed. Conversely, homosynaptic long-term depression would cause other synapses to potentiate in a manner which keeps the average synaptic weight approximately conserved. The scope of these changes could be global or compartmentalized in the dendrites.

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