ArticlePloS one2011
The depolarizing action of GABA in cultured hippocampal neurons is not due to the absence of ketone bodies.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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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.
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Who cites it
5 citing papers in PubMed, 6 citations in OpenAlex.
- Direct type I IFN but not MDA5/TLR3 activation of dendritic cells is required for maturation and metabolic shift to glycolysis after poly IC stimulation.PLoS biology · 2014Article
- Developmental and maintenance defects in Rett syndrome neurons identified by a new mouse staging system in vitro.Frontiers in cellular neuroscience · 2014Article
- The influence of stress at puberty on mood and learning: role of the α4βδ GABAA receptor.Neuroscience · 2013Review
- Kinases SPAK and OSR1 are upregulated by estradiol and activate NKCC1 in the developing hypothalamus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- Refuting the challenges of the developmental shift of polarity of GABA actions: GABA more exciting than ever!Frontiers in cellular neuroscience · 2012Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Two recent reports propose that the depolarizing action of GABA in the immature brain is an artifact of in vitro preparations in which glucose is the only energy source. The authors argue that this does not mimic the physiological environment because the suckling rats use ketone bodies and pyruvate as major sources of metabolic energy. Here, we show that availability of physiologically relevant levels of ketone bodies has no impact on the excitatory action of GABA in immature cultured hippocampal neurons. Addition of β-hydroxybutyrate (BHB), the primary ketone body in the neonate rat, affected neither intracellular calcium elevation nor membrane depolarizations induced by the GABA-A receptor agonist muscimol, when assessed with calcium imaging or perforated patch-clamp recording, respectively. These results confirm that the addition of ketone bodies to the extracellular environment to mimic conditions in the neonatal brain does not reverse the chloride gradient and therefore render GABA hyperpolarizing. Our data are consistent with the existence of a genuine "developmental switch" mechanism in which GABA goes from having a predominantly excitatory role in immature cells to a predominantly inhibitory one in adults.
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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.