Abstract
Inhibitory transmission through the neurotransmitter γ-aminobutyric acid (GABA) shapes network activity in the mammalian cerebral cortex by filtering synaptic incoming information and dictating the activity of principal cells. The incredibly diverse population of cortical neurons that use GABA as neurotransmitter shows an equally diverse range of mechanisms that regulate changes in the strength of GABAergic synaptic transmission and allow them to dynamically follow and command the activity of neuronal ensembles. Similarly to glutamatergic synaptic transmission, activity-dependent functional changes in inhibitory neurotransmission are accompanied by alterations in GABAergic synapse structure that range from morphological reorganization of postsynaptic density to de novo formation and elimination of inhibitory contacts. Here we review several aspects of structural plasticity of inhibitory synapses, including its induction by different forms of neuronal activity, behavioral and sensory experience and the molecular mechanisms and signaling pathways involved. We discuss the functional consequences of GABAergic synapse structural plasticity for information processing and memory formation in view of the heterogenous nature of the structural plasticity phenomena affecting inhibitory synapses impinging on somatic and dendritic compartments of cortical and hippocampal neurons.
Highlights
CELLULAR NEUROSCIENCEShaping inhibition: activity dependent structural plasticity of GABAergic synapses. Department of Basic Neuroscience, Geneva Medical Center, University of Geneva, Geneva, Switzerland
GABAERGIC SYSTEM AS A SUBSTRATE FOR BRAIN PLASTICITY During the last decades neuroscientists and physiologists worldwide have made an herculean effort to elucidate the mechanisms of activity-driven changes in synaptic strength and understand its physiological significance as the brain substrate for learning and memory (Malenka and Bear, 2004; Mayford et al, 2012)
In vivo studies have shown that dendritic spines, the morphological correlate of glutamatergic synapses in excitatory neurons, are formed and eliminated in response to synaptic activity patterns induced by learning behavior (Xu et al, 2009) and that formation of durable memories is directly correlated with the stability and formation of new excitatory synapses (Yang et al, 2009)
Summary
Shaping inhibition: activity dependent structural plasticity of GABAergic synapses. Department of Basic Neuroscience, Geneva Medical Center, University of Geneva, Geneva, Switzerland. Inhibitory transmission through the neurotransmitter γ-aminobutyric acid (GABA) shapes network activity in the mammalian cerebral cortex by filtering synaptic incoming information and dictating the activity of principal cells. The incredibly diverse population of cortical neurons that use GABA as neurotransmitter shows an diverse range of mechanisms that regulate changes in the strength of GABAergic synaptic transmission and allow them to dynamically follow and command the activity of neuronal ensembles. To glutamatergic synaptic transmission, activity-dependent functional changes in inhibitory neurotransmission are accompanied by alterations in GABAergic synapse structure that range from morphological reorganization of postsynaptic density to de novo formation and elimination of inhibitory contacts. We review several aspects of structural plasticity of inhibitory synapses, including its induction by different forms of neuronal activity, behavioral and sensory experience and the molecular mechanisms and signaling pathways involved.
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