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Activity-dependent regulation of inhibitory synaptic transmission in hippocampal neurons
Abstract
Neural activity regulates the number and properties of GABAergic synapses in the brain, but the mechanisms underlying these changes are unclear. We found that blocking spike activity globally in developing hippocampal neurons from rats reduced the density of GABAergic terminals as well as the frequency and amplitude of miniature inhibitory postsynaptic currents (mIPSCs). Chronic inactivity later in development led to a reduction in the mIPSC amplitude, without any change in GABAergic synapse density. By contrast, hyperpolarizing or abolishing spike activity in single neurons did not alter GABAergic synaptic inputs. Suppressing activity in individual presynaptic GABAergic neurons also failed to decrease synaptic output. Our results indicate that GABAergic synapses are regulated by the level of activity in surrounding neurons. Notably, we found that the expression of GABAergic plasticity involves changes in the amount of neurotransmitter in individual vesicles.
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“Consistent with the idea that inhibitory scaling might result from release of a secreted factor during changes in network activity, scaling of inhibitory synapses cannot be induced by hyperpolarization of individual presynaptic or postsynaptic neurons (Hartman et al. 2006).”
From Homeostatic Synaptic Plasticity: Local and Global Mechanisms for Stabilizing Neuronal Function (2012) · cites this paper as Hartman et al. 2006
In the citing paper
“Interestingly, both in vitro and in vivo studies have documented that homeostatic regulation of inhibition involves coordinated changes in postsynaptic strength, synapse number, and likely presynaptic release probability (Kilman et al. 2002;Maffei et al. 2004;Hartman et al. 2006).”
From Homeostatic Synaptic Plasticity: Local and Global Mechanisms for Stabilizing Neuronal Function (2012) · cites this paper as Hartman et al. 2006
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“Curiously, the age-dependency of quantal responses has been demonstrated in dissociated cultures (e.g. Burrone et al., 2002; Han and Stevens, 2009; Hartman et al., 2006; Wierenga et al., 2006), albeit not necessarily in the same direction.”
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Metadata
- Authors
- Hartman, K. N., Pal, S. K., Burrone, J., & Murthy, V. N.
- Affiliations
- Harvard University (US)
- Corresponding author
- Murthy, Venkatesh N
- Venue
- Nature Neuroscience
- Published
- 2006-04-02
- Volume
- 9
- Issue
- 5
- Pages
- 642-649
- ISSN
- 1097-6256 (ISSN-L)
- 1546-1726
- OpenAlex
- W2156087438
- Cited by
- 221
- References
- 0
- Citations by year
- 2026: 3 · 2025: 6 · 2024: 10 · 2023: 9 · 2022: 4 · 2021: 9 · 2020: 11 · 2019: 10 · 2018: 9 · 2017: 10 · 2016: 9 · 2015: 14 · 2014: 12 · 2013: 25 · 2012: 11
- FWCI
- 5.53
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- Research Portal (King's College London) (submittedVersion)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Cognitive Neuroscience › Neural dynamics and brain function
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Keywords
- activity-dependent synaptic plasticity, GABAergic synapses, synaptic inhibition, miniature inhibitory postsynaptic currents, hippocampal neurons, synaptic density, presynaptic inhibition, neuronal activity regulation
- MeSH terms
- Animals, Animals, Newborn, Carrier Proteins, Cells, Cultured, Drug Interactions, Electric Stimulation, Glutamate Decarboxylase, Hippocampus, Isoenzymes, Membrane Potentials, Membrane Proteins, Microtubule-Associated Proteins, Neural Inhibition, Synaptic Transmission, Neurons, Phosphinic Acids, Pyridines, Tetrodotoxin, Transfection, Patch-Clamp Techniques, Potassium Channels, Inwardly Rectifying, Vesicular Glutamate Transport Protein 1, Rats
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