ArticleThe Journal of pharmacology and experimental therapeutics2008
Ethanol decreases Purkinje neuron excitability by increasing GABA release in rat cerebellar slices.
Article in The Journal of pharmacology and experimental therapeutics, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 50 citations in OpenAlex.
- Article
- Chronic Ethanol Exposure Enhances Facial Stimulation-Evoked Mossy Fiber-Granule Cell Synaptic TransmissionFrontiers in systems neuroscience · 2021Article
- Cocaine withdrawal reduces GABAThe European journal of neuroscience · 2019Article
- Supplement of Betaine into Embryo Culture Medium Can Rescue Injury Effect of Ethanol on Mouse Embryo Development.Scientific reports · 2018Article
- Chronic Ethanol Consumption Impairs the Tactile-Evoked Long-Term Depression at Cerebellar Molecular Layer Interneuron-Purkinje Cell SynapsesFrontiers in cellular neuroscience · 2018Article
- Ethanol Modulates the Spontaneous Complex Spike Waveform of Cerebellar Purkinje Cells RecordedFrontiers in cellular neuroscience · 2017Article
- Ethanol modulates facial stimulation-evoked outward currents in cerebellar Purkinje cells in vivo in mice.Scientific reports · 2016Article
- Essential Tremor: What We Can Learn from Current Pharmacotherapy.Tremor and other hyperkinetic movements (New York, N.Y.) · 2016Review
- Mini-Review: Effects of Ethanol on GABAA Receptor-Mediated Neurotransmission in the Cerebellar Cortex--Recent Advances.Cerebellum (London, England) · 2015Review
- Ethanol and corticotropin releasing factor receptor modulation of central amygdala neurocircuitry: An update and future directions.Alcohol (Fayetteville, N.Y.) · 2015Review
- Characterization of activity-dependent changes in flavoprotein fluorescence in cerebellar slices from juvenile rats.Neuroscience letters · 2015Article
- GABAA receptor-mediated tonic depolarization in developing neural circuits.Molecular neurobiology · 2014Review
- Ethanol affects NMDA receptor signaling at climbing fiber-Purkinje cell synapses in mice and impairs cerebellar LTD.Journal of neurophysiology · 2013Article
- Independent contributions of alcohol and stress axis hormones to painful peripheral neuropathy.Neuroscience · 2013Article
- Response to ethanol induced ataxia between C57BL/6J and 129X1/SvJ mouse strains using a treadmill based assay.Pharmacology, biochemistry, and behavior · 2013Article
- Ethanol modulation of synaptic plasticity.Neuropharmacology · 2011Review
- Activation of steroid-sensitive TRPM3 channels potentiates glutamatergic transmission at cerebellar Purkinje neurons from developing rats.Journal of neurochemistry · 2011Article
- Augmented central nitric oxide production inhibits vasopressin release during hemorrhage in acute alcohol-intoxicated rodents.American journal of physiology. Regulatory, integrative and comparative physiology · 2011Article
- Opposite effects of acute ethanol exposure on GAP-43 and BDNF expression in the hippocampus versus the cerebellum of juvenile rats.Alcohol (Fayetteville, N.Y.) · 2011Article
- Chronic ethanol and withdrawal differentially modulate lateral/basolateral amygdala paracapsular and local GABAergic synapses.The Journal of pharmacology and experimental therapeutics · 2011Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Cerebellar Purkinje neurons (PNs) receive inhibitory GABAergic input from stellate and basket cells, which are located in the outer and inner portions of the molecular layer, respectively. Ethanol (EtOH) was recently shown to increase GABAergic transmission at PNs via a mechanism that involves enhanced calcium release from presynaptic internal stores (J Pharmacol Exp Ther 323:356-364, 2007). Here, we further characterized the effect of EtOH on GABA release and assessed its impact on PN excitability. Using whole-cell patch-clamp electrophysiological techniques in cerebellar vermis parasagittal slices, we found that EtOH acutely increases the frequency but not the amplitude or half-width of miniature and spontaneous inhibitory postsynaptic currents (IPSCs). EtOH significantly increased the amplitude and decreased the paired pulse ratio of IPSCs evoked by stimulation in the outer but not inner molecular layer. In current clamp, EtOH decreased both the amplitude of excitatory postsynaptic potentials evoked in PNs by granule cell axon stimulation and the number of action potentials triggered by these events; these effects depended on GABA(A) receptor activation because they were not observed in presence of bicuculline. Loose-patch cell-attached PN recordings revealed that neither the spontaneous action potential firing frequency nor the coefficient of variation of the interspike interval was altered by acute EtOH exposure. These findings suggest that EtOH differentially affects GABAergic transmission at stellate cell- and basket cell-to-PN synapses and that it modulates PN firing triggered by granule cell axonal input. These effects could be in part responsible for the cerebellar impairments associated with acute EtOH intoxication.
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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.