ArticleAlcoholism, clinical and experimental research2012
Excitation of rat cerebellar Golgi cells by ethanol: further characterization of the mechanism.
Article in Alcoholism, clinical and experimental research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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
15 citing papers in PubMed, 21 citations in OpenAlex.
- The Cerebellar GABAHandbook of experimental pharmacology · 2018Article
- Recreational concentrations of alcohol enhance synaptic inhibition of cerebellar unipolar brush cells via pre- and postsynaptic mechanisms.Journal of neurophysiology · 2017Article
- Sensitivity of GABAergic Tonic Currents to Acute Ethanol in Cerebellar Granule Neurons is Not Age- or δ Subunit-Dependent in Developing Rats.Alcoholism, clinical and experimental research · 2016Article
- Mini-Review: Effects of Ethanol on GABAA Receptor-Mediated Neurotransmission in the Cerebellar Cortex--Recent Advances.Cerebellum (London, England) · 2015Review
- Ethanol-Induced Cerebellar Ataxia: Cellular and Molecular Mechanisms.Cerebellum (London, England) · 2015Article
- Simulation of alcohol action upon a detailed Purkinje neuron model and a simpler surrogate model that runs >400 times faster.BMC neuroscience · 2015Article
- Apoptosis of Purkinje and granular cells of the cerebellum following chronic ethanol intake.Cerebellum (London, England) · 2014Article
- Repeated intermittent alcohol exposure during the third trimester-equivalent increases expression of the GABA(A) receptor δ subunit in cerebellar granule neurons and delays motor development in rats.Neuropharmacology · 2014Article
- Neuronal oscillations in Golgi cells and Purkinje cells are accompanied by decreases in Shannon information entropy.Cerebellum (London, England) · 2014Article
- Acute ethanol exposure inhibits silencing of cerebellar Golgi cell firing induced by granule cell axon input.Frontiers in integrative neuroscience · 2014Article
- Opposite actions of alcohol on tonic GABA(A) receptor currents mediated by nNOS and PKC activity.Nature neuroscience · 2013Article
- Primate cerebellar granule cells exhibit a tonic GABAAR conductance that is not affected by alcohol: a possible cellular substrate of the low level of response phenotype.Frontiers in neural circuits · 2013Article
- A reinforcing circuit action of extrasynaptic GABAA receptor modulators on cerebellar granule cell inhibition.PloS one · 2013Article
- Article
- Acute ethanol exposure increases firing and induces oscillations in cerebellar Golgi cells of freely moving rats.Alcoholism, clinical and experimental research · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundStudies with rodents suggest that acute ethanol exposure impairs information flow through the cerebellar cortex, in part, by increasing GABAergic input to granule cells. Experiments suggest that an increase in the excitability of specialized GABAergic interneurons that regulate granule cell activity (i.e., Golgi cells [GoCs]) contributes to this effect. In GoCs, ethanol increases spontaneous action potential firing frequency, decreases the afterhyperpolarization amplitude, and depolarizes the membrane potential. Studies suggest that these effects could be mediated by inhibition of the Na(+)/K(+) ATPase. The purpose of this study was to characterize the potential role of other GoC conductances in the mechanism of action of ethanol.
methodsComputer modeling techniques and patch-clamp electrophysiological recordings with acute slices from rat cerebella were used for these studies.
resultsComputer modeling suggested that modulation of subthreshold Na(+) channels, hyperpolarization-activated currents, and several K(+) conductances could explain some but not all actions of ethanol on GoCs. Electrophysiological studies did not find evidence consistent with a contribution of these conductances. Quinidine, a nonselective blocker of several types of channels (including several K(+) channels) that also antagonizes the Na(+)/K(+) ATPase, reduced the effect of ethanol on GoC firing.
conclusionsThese findings further support that ethanol increases GoC excitability via modulation of the Na(+)/K(+) ATPase and suggest that a quinidine-sensitive K(+) channel may also play a role in the mechanism of action of ethanol.
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.