Forms and Mechanisms of Homeostatic Synaptic Plasticity
Long-term changes of neuronal network activity level result in the activity of excitatory and inhibitory synapses counteracting the change of the mean frequency of spike generation and contributing to network homeostasis maintenance. The review describes the manifestations of homeostatic synaptic plasticity in vivo and in vitro. The best investigated form of homeostatic synaptic plasticity, or “synaptic scaling” is the change of synapse intensity between excitatory neurons, multiple of initial synapse intensity and inversely proportional to the change of the frequency of spikes in postsynaptic neurons. However, the intensity of inhibitory synapses on excitatory neurons, as well as the intensity of excitatory synapses on inhibitory neurons, change directly proportionally to the change of spike frequency. There has been considered the central postsynaptic mechanism participating in the occurrence and further regulation of homeostatic plasticity of excitatory synapses — the alteration of the pool of α-amino-3-hydroxy-5-methyl-4-isoxasolpropionic acid receptors (AMPA-receptors). There have been characterized presynaptic molecular mechanisms and considered the role of concentration changes of intracellular calcium, molecules of cytoadherence, and the secretion of signal molecules in postsynaptic regulation of homeostatic plasticity.
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