Abstract
The problem of frequency coding is closely related to the studies of inhibitory transmission as a factor of neural network plasticity. The rewiew presents basic mechanisms of inhibitory control of spatio-temporal pattern of neural activity during signal processing. Current views are analyzed in respect of dynamic synapses, their instability and variation within the ongoing activity. The results presented here demonstrate that short-term plasticity operates with the combined contribution of excitatory and inhibitory synapses. The role of GABAergic potentials in modulation of intracellular messenger’s activity is discussed, including those implicated in postsynaptic modifications of excitatory and inhibitory transmission. The main topics concerning the molecular mechanisms centered on the lateral diffusion of GABAA receptors. The data of many reports argue for coordinating role of actin cytoskeleton. It is proposed that postsynaptic mechanisms underlying GABAA plasticity may be activated in result of fast adaptation of actin cytoskeleton and associated proteins to disbalance between excitation and inhibition.
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