ArticleJournal of neurophysiology2008
The role of protein kinase A in the ethanol-induced increase in spontaneous GABA release onto cerebellar Purkinje neurons.
Article in Journal of neurophysiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 53 citations in OpenAlex.
- Synaptic Effects Induced by Alcohol.Current topics in behavioral neurosciences · 2025Review
- The Synaptic Interactions of Alcohol and the Endogenous Cannabinoid System.Alcohol research : current reviews · 2022Review
- Ethanol induces persistent potentiation of 5-HTNeuropharmacology · 2021Article
- Apremilast regulates acute effects of ethanol and other GABAergic drugs via protein kinase A-dependent signaling.Neuropharmacology · 2020Article
- Differential sensitivity of human neurons carrying μ opioid receptor (MOR) N40D variants in response to ethanol.Alcohol (Fayetteville, N.Y.) · 2020Article
- Endocannabinoid Signaling in the Central Amygdala and Bed Nucleus of the Stria Terminalis: Implications for the Pathophysiology and Treatment of Alcohol Use Disorder.Alcoholism, clinical and experimental research · 2019Review
- Distinct functions of endogenous cannabinoid system in alcohol abuse disorders.British journal of pharmacology · 2019Review
- Forensic appraisal of death due to acute alcohol poisoning: three case reports and a literature review.Forensic sciences research · 2019Article
- IL-1β expression is increased and regulates GABA transmission following chronic ethanol in mouse central amygdala.Brain, behavior, and immunity · 2019Article
- The Cerebellar GABAHandbook of experimental pharmacology · 2018Article
- Ethanol Stimulates Locomotion via a GGenetics · 2017Article
- Synaptic targets: Chronic alcohol actions.Neuropharmacology · 2017Review
- Chronic alcohol exposure disrupts CBAddiction biology · 2017Article
- 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
- Chronic ethanol exposure decreases CB1 receptor function at GABAergic synapses in the rat central amygdala.Addiction biology · 2016Article
- Interactions between ethanol and the endocannabinoid system at GABAergic synapses on basolateral amygdala principal neurons.Alcohol (Fayetteville, N.Y.) · 2015Article
- Phosphodiesterase regulation of alcohol drinking in rodents.Alcohol (Fayetteville, N.Y.) · 2015Review
- Ethanol Activation of PKA Mediates Single-Minded 2 Expression in Neuronal Cells.Molecular neurobiology · 2015Article
- Electrophysiological and Immunohistochemical Evidence for an Increase in GABAergic Inputs and HCN Channels in Purkinje Cells that Survive Developmental Ethanol Exposure.Cerebellum (London, England) · 2015Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Ethanol increases miniature inhibitory postsynaptic current frequency and decreases the paired-pulse ratio, which suggests that ethanol increases both spontaneous and evoked GABA release, respectively. We have shown previously that ethanol increases GABA release at the rat interneuron-Purkinje cell synapse and that this ethanol effect involves calcium release from internal stores; however, further exploration of the mechanism responsible for ethanol-enhanced GABA release was needed. We found that a cannabinoid receptor 1 (CB1) agonist, WIN-55212, and a GABA(B) receptor agonist, baclofen, decreased baseline spontaneous GABA release and prevented ethanol from increasing spontaneous GABA release. The CB1 receptor and GABA(B) receptor are Galpha i-linked G protein-coupled receptors with common downstream messengers that include adenylate cyclase and protein kinase A (PKA). Adenylate cyclase and PKA antagonists blocked ethanol from increasing spontaneous GABA release, whereas a PKA antagonist limited to the postsynaptic neuron did not block ethanol from increasing spontaneous GABA release. These results suggest that presynaptic PKA plays an essential role in ethanol-enhanced spontaneous GABA release. Similar to ethanol, we found that the mechanism of the cannabinoid-mediated decrease in spontaneous GABA release involves internal calcium stores and PKA. A PKA antagonist decreased baseline spontaneous GABA release. This effect was reduced after incubating the slice with a calcium chelator, BAPTA-AM, but was unaffected when BAPTA was limited to the postsynaptic neuron. This suggests that the PKA antagonist is acting through a presynaptic, calcium-dependent mechanism to decrease spontaneous GABA release. Overall, these results suggest that PKA activation is necessary for ethanol to increase spontaneous GABA release.
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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.