ArticleProceedings of the National Academy of Sciences of the United States of America2008
GABAA transmission is a critical step in the process of triggering homeostatic increases in quantal amplitude.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 47 citations in OpenAlex.
- The effect of repetitive transcranial magnetic stimulation on gamma oscillatory activity in schizophrenia.PloS one · 2011Trial
- APOE4 and doxorubicin impair inhibitory interneuron function and homeostatic regulation in the entorhinal cortex.PloS one · 2026Article
- Chloride Modulates Central pH Sensitivity and Plasticity of Brainstem Breathing-Related Biorhythms in Zebra Finch Embryos.Developmental psychobiology · 2024Article
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- Forebrain E-I balance controlled in cognition through coordinated inhibition and inhibitory transcriptome mechanism.Frontiers in cellular neuroscience · 2023Article
- The Uniform and Nonuniform Nature of Slow and Rapid Scaling in Embryonic Motoneurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Homeostatic Regulation of Motoneuron Properties in Development.Advances in neurobiology · 2022Review
- Sustained treatment with an α5 GABA A receptor negative allosteric modulator delays excitatory circuit development while maintaining GABAergic neurotransmission.Neuropharmacology · 2021Article
- FMRP attenuates activity dependent modifications in the mitochondrial proteome.Molecular brain · 2021Article
- Intrinsic plasticity and birdsong learning.Neurobiology of learning and memory · 2021Review
- Regulation of synaptic scaling by action potential-independent miniature neurotransmission.Journal of neuroscience research · 2018Review
- Developmental Disruption of Recurrent Inhibitory Feedback Results in Compensatory Adaptation in the Renshaw Cell-Motor Neuron Circuit.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Spontaneous Release Regulates Synaptic Scaling in the Embryonic Spinal Network In Vivo.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- Glycinergic Neurotransmission: A Potent Regulator of Embryonic Motor Neuron Dendritic Morphology and Synaptic Plasticity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- Decreased spinal synaptic inputs to phrenic motor neurons elicit localized inactivity-induced phrenic motor facilitation.Experimental neurology · 2014Article
- GABAA receptor-mediated tonic depolarization in developing neural circuits.Molecular neurobiology · 2014Review
- Homeostatic synaptic plasticity in developing spinal networks driven by excitatory GABAergic currents.Neuropharmacology · 2014Review
- Article
- In vivo synaptic scaling is mediated by GluA2-lacking AMPA receptors in the embryonic spinal cord.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
When activity levels are altered over days, a network of cells is capable of recognizing this perturbation and triggering several distinct compensatory changes that should help to recover and maintain the original activity levels homeostatically. One feature commonly observed after activity blockade has been a compensatory increase in excitatory quantal amplitude. The sensing machinery that detects altered activity levels is a central focus of the field currently, but thus far it has been elusive. The vast majority of studies that reduce network activity also reduce neurotransmission. We address the possibility that reduced neurotransmission can trigger increases in quantal amplitude. In this work, we blocked glutamatergic or GABA(A) transmission in ovo for 2 days while maintaining relatively normal network activity. We found that reducing GABA(A) transmission triggered compensatory increases in both GABA and AMPA quantal amplitude in embryonic spinal motoneurons. Glutamatergic blockade had no effect on quantal amplitude. Therefore, GABA binding to the GABA(A) receptor appears to be a critical step in the sensing machinery for homeostatic synaptic plasticity. The findings suggest that homeostatic increases in quantal amplitude may normally be triggered by reduced levels of activity, which are sensed in the developing spinal cord by GABA, via the GABA(A) receptor. Therefore, GABA appears to be serving as a proxy for activity levels.
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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.