ArticleFrontiers in synaptic neuroscience2010
Spike-timing dependent plasticity in inhibitory circuits.
Article in Frontiers in synaptic neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 70 citations in OpenAlex.
- Linking neuron-axon-synapse architecture to white matter vasculature using high-resolution multimodal MRI in primate brain.Imaging neuroscience (Cambridge, Mass.) · 2025Article
- A manifold neural population code for space in hippocampal coactivity dynamics independent of place fields.Cell reports · 2023Article
- Pre- and postsynaptically expressed spike-timing-dependent plasticity contribute differentially to neuronal learning.PLoS computational biology · 2022Article
- NKCC1 and KCC2: Structural insights into phospho-regulation.Frontiers in molecular neuroscience · 2022Review
- All-or-none disconnection of pyramidal inputs onto parvalbumin-positive interneurons gates ocular dominance plasticity.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Striatal Chloride Dysregulation and Impaired GABAergic Signaling Due to Cation-Chloride Cotransporter Dysfunction in Huntington's Disease.Frontiers in cellular neuroscience · 2021Review
- Effect of interpopulation spike-timing-dependent plasticity on synchronized rhythms in neuronal networks with inhibitory and excitatory populations.Cognitive neurodynamics · 2020Article
- Burst synchronization in a scale-free neuronal network with inhibitory spike-timing-dependent plasticity.Cognitive neurodynamics · 2019Article
- A biophysical model of dynamic balancing of excitation and inhibition in fast oscillatory large-scale networks.PLoS computational biology · 2018Article
- Emerging Mechanisms Underlying Dynamics of GABAergic Synapses.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Review
- Balanced excitation and inhibition are required for high-capacity, noise-robust neuronal selectivity.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Correlation-based model of artificially induced plasticity in motor cortex by a bidirectional brain-computer interface.PLoS computational biology · 2017Article
- Dynamic Hebbian Cross-Correlation Learning Resolves the Spike Timing Dependent Plasticity Conundrum.Frontiers in computational neuroscience · 2017Article
- Synapse-specific expression of calcium-permeable AMPA receptors in neocortical layer 5.The Journal of physiology · 2016Article
- Self-organization in Balanced State Networks by STDP and Homeostatic Plasticity.PLoS computational biology · 2015Article
- Plasticity of cortical excitatory-inhibitory balance.Annual review of neuroscience · 2015Review
- Article
- K-Cl cotransporter KCC2--a moonlighting protein in excitatory and inhibitory synapse development and function.Pflugers Archiv : European journal of physiology · 2015Review
- Mixed signal learning by spike correlation propagation in feedback inhibitory circuits.PLoS computational biology · 2015Article
- Kainate receptors coexist in a functional complex with KCC2 and regulate chloride homeostasis in hippocampal neurons.Cell reports · 2014Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Inhibitory circuits in the brain rely on GABA-releasing interneurons. For long, inhibitory circuits were considered weakly plastic in the face of patterns of neuronal activity that trigger long-term changes in the synapses between excitatory principal cells. Recent studies however have shown that GABAergic circuits undergo various forms of long-term plasticity. For the purpose of this review, we identify three major long-term plasticity expression sites. The first locus is the glutamatergic synapses that excite GABAergic inhibitory cells and drive their activity. Such synapses, on many but not all inhibitory interneurons, exhibit long-term potentiation (LTP) and depression (LTD). Second, GABAergic synapses themselves can undergo changes in GABA release probability or postsynaptic GABA receptors. The third site of plasticity is in the postsynaptic anion gradient of GABAergic synapses; coincident firing of GABAergic axons and postsynaptic neurons can cause a long-lasting change in the reversal potential of GABA(A) receptors mediating fast inhibitory postsynaptic potentials. We review the recent literature on these forms of plasticity by asking how they may be triggered by specific patterns of pre- and postsynaptic action potentials, although very few studies have directly examined spike-timing dependent plasticity (STDP) protocols in inhibitory circuits. Plasticity of interneuron recruitment and of GABAergic signaling provides for a rich flexibility in inhibition that may be central to many aspects of brain function. We do not consider plasticity at glutamatergic synapses on Purkinje cells and other GABAergic principal cells.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.