ArticleProceedings of the National Academy of Sciences of the United States of America2009
Compensatory changes in cellular excitability, not synaptic scaling, contribute to homeostatic recovery of embryonic network activity.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 50 citations in OpenAlex.
- Article
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- Homeostatic Regulation of Motoneuron Properties in Development.Advances in neurobiology · 2022Review
- Prenatal exposure to nicotine disrupts synaptic network formation by inhibiting spontaneous correlated wave activity.IBRO reports · 2020Article
- Differential neuropeptide modulation of premotor and motor neurons in the lobster cardiac ganglion.Journal of neurophysiology · 2020Article
- Canard-induced complex oscillations in an excitatory network.Journal of mathematical biology · 2020Article
- Homeostatic Intrinsic Plasticity Is Functionally Altered in Fmr1 KO Cortical Neurons.Cell reports · 2019Article
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- 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
- Elevated intracellular NaJournal of neurochemistry · 2017Article
- Clarithromycin increases neuronal excitability in CA3 pyramidal neurons through a reduction in GABAergic signaling.Journal of neurophysiology · 2017Article
- The Effects of GABAergic Polarity Changes on Episodic Neural Network Activity in Developing Neural Systems.Frontiers in computational neuroscience · 2017Article
- Article
- 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
- Depolarizing GABA and developmental epilepsies.CNS neuroscience & therapeutics · 2015Review
- Spinal NMDA receptor activation constrains inactivity-induced phrenic motor facilitation in Charles River Sprague-Dawley rats.Journal of applied physiology (Bethesda, Md. : 1985) · 2014Article
- Homeostatic synaptic plasticity in developing spinal networks driven by excitatory GABAergic currents.Neuropharmacology · 2014Review
- Optogenetic-mediated increases in in vivo spontaneous activity disrupt pool-specific but not dorsal-ventral motoneuron pathfinding.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
When neuronal activity is reduced over a period of days, compensatory changes in synaptic strength and/or cellular excitability are triggered, which are thought to act in a manner to homeostatically recover normal activity levels. The time course over which changes in homeostatic synaptic strength and cellular excitability occur are not clear. Although many studies show that 1-2 days of activity block are necessary to trigger increases in excitatory quantal strength, few studies have been able to examine whether these mechanisms actually underlie recovery of network activity. Here, we examine the mechanisms underlying recovery of embryonic motor activity following block of either excitatory GABAergic or glutamatergic inputs in vivo. We find that GABA(A) receptor blockade triggers fast changes in cellular excitability that occur during the recovery of activity but before changes in synaptic scaling. This increase in cellular excitability is mediated in part by an increase in sodium currents and a reduction in the fast-inactivating and calcium-activated potassium currents. These findings suggest that compensatory changes in cellular excitability, rather than synaptic scaling, contribute to activity recovery. Further, we find a special role for the GABA(A) receptor in triggering several homeostatic mechanisms after activity perturbations, including changes in cellular excitability and GABAergic and AMPAergic synaptic strength. The temporal difference in expression of homeostatic changes in cellular excitability and synaptic strength suggests that there are multiple mechanisms and pathways engaged to regulate network activity, and that each may have temporally distinct functions.
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