ArticleProceedings of the National Academy of Sciences of the United States of America2015
GABAB receptor deficiency causes failure of neuronal homeostasis in hippocampal networks.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
32 citing papers in PubMed, 57 citations in OpenAlex.
- A semi-automated MEA spike sorting method for high-throughput assessment of cultured neurons.Stem cell reports · 2026Article
- Modeling presynaptic inhibition by the amyloid precursor protein demonstrates one potential mechanism for preventing runaway synaptic modification in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Regulation of presynaptic homeostatic plasticity by glial signalling in Alzheimer's disease.The Journal of physiology · 2025Review
- Taurine Attenuates Neuronal Ferroptosis by CSF-Derived Exosomes of GABABR Encephalitis Through GABABR/NF2/P-YAP Pathway.Molecular neurobiology · 2025Article
- Genetic implication of GABAFrontiers in pharmacology · 2025Review
- N-acetyltransferase 10 mediates cognitive dysfunction through the acetylation of GABAProceedings of the National Academy of Sciences of the United States of America · 2024Article
- Linking activity dyshomeostasis and sleep disturbances in Alzheimer disease.Nature reviews. Neuroscience · 2024Review
- Designing Electrical Stimulation Platforms for Neural Cell Cultivation Using Poly(aniline): Camphorsulfonic Acid.Polymers · 2023Review
- IGF-1 receptor regulates upward firing rate homeostasis via the mitochondrial calcium uniporter.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- GABACurrent neuropharmacology · 2022Review
- Keeping the Balance: GABABrain sciences · 2022Review
- Disrupted neural correlates of anesthesia and sleep reveal early circuit dysfunctions in Alzheimer models.Cell reports · 2022Article
- Excitatory and inhibitory hippocampal neurons differ in their homeostatic adaptation to chronic M-channel modulation.Frontiers in molecular neuroscience · 2022Article
- Mechanisms and Regulation of Neuronal GABACurrent topics in behavioral neurosciences · 2022Review
- CK2 Phosphorylation Is Required for Regulation of Syntaxin 1A Activity in CaInternational journal of molecular sciences · 2021Article
- Npas4a expression in the teleost forebrain is associated with stress coping style differences in fear learning.Scientific reports · 2021Article
- GABAFrontiers in cellular neuroscience · 2021Article
- M-Current Inhibition in Hippocampal Excitatory Neurons Triggers Intrinsic and Synaptic Homeostatic Responses at Different Temporal Scales.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Article
- Mitochondrial Regulation of the Hippocampal Firing Rate Set Point and Seizure Susceptibility.Neuron · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 2 institutions in 2 countries.
Funding
Abstract
Stabilization of neuronal activity by homeostatic control systems is fundamental for proper functioning of neural circuits. Failure in neuronal homeostasis has been hypothesized to underlie common pathophysiological mechanisms in a variety of brain disorders. However, the key molecules regulating homeostasis in central mammalian neural circuits remain obscure. Here, we show that selective inactivation of GABAB, but not GABA(A), receptors impairs firing rate homeostasis by disrupting synaptic homeostatic plasticity in hippocampal networks. Pharmacological GABA(B) receptor (GABA(B)R) blockade or genetic deletion of the GB(1a) receptor subunit disrupts homeostatic regulation of synaptic vesicle release. GABA(B)Rs mediate adaptive presynaptic enhancement to neuronal inactivity by two principle mechanisms: First, neuronal silencing promotes syntaxin-1 switch from a closed to an open conformation to accelerate soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) complex assembly, and second, it boosts spike-evoked presynaptic calcium flux. In both cases, neuronal inactivity removes tonic block imposed by the presynaptic, GB(1a)-containing receptors on syntaxin-1 opening and calcium entry to enhance probability of vesicle fusion. We identified the GB(1a) intracellular domain essential for the presynaptic homeostatic response by tuning intermolecular interactions among the receptor, syntaxin-1, and the Ca(V)2.2 channel. The presynaptic adaptations were accompanied by scaling of excitatory quantal amplitude via the postsynaptic, GB(1b)-containing receptors. Thus, GABA(B)Rs sense chronic perturbations in GABA levels and transduce it to homeostatic changes in synaptic strength. Our results reveal a novel role for GABA(B)R as a key regulator of population firing stability and propose that disruption of homeostatic synaptic plasticity may underlie seizure's persistence in the absence of functional GABA(B)Rs.
Indexed as
Identifiers
What OpenQuestion holds
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.