ArticlePloS one2009
Adenylyl cyclases 1 and 8 initiate a presynaptic homeostatic response to ethanol treatment.
Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 28 citations in OpenAlex.
- Synaptic Mechanisms of Ethanol Tolerance and Neuroplasticity: Insights from Invertebrate Models.International journal of molecular sciences · 2024Review
- Homeostatic control of Drosophila neuromuscular junction function.Synapse (New York, N.Y.) · 2020Review
- Calcium/calmodulin-stimulated adenylyl cyclases 1 and 8 regulate reward-related brain activity and ethanol consumption.Brain imaging and behavior · 2019Article
- Cross-Species Co-analysis of Prefrontal Cortex Chronic Ethanol Transcriptome Responses in Mice and Monkeys.Frontiers in molecular neuroscience · 2019Article
- Adenylyl Cyclase 1 Is Required for Ethanol-Induced Locomotor Sensitization and Associated Increases in NMDA Receptor Phosphorylation and Function in the Dorsal Medial Striatum.The Journal of pharmacology and experimental therapeutics · 2017Article
- Ethanol Stimulates Locomotion via a GGenetics · 2017Article
- Myelin-targeted, texaphyrin-based multimodal imaging agent for magnetic resonance and optical imaging.Contrast media & molecular imaging · 2016Article
- Deficits in behavioral sensitization and dopaminergic responses to methamphetamine in adenylyl cyclase 1/8-deficient mice.Journal of neurochemistry · 2015Article
- Activation of α7 nicotinic acetylcholine receptors increases intracellular cAMP levels via activation of AC1 in hippocampal neurons.Neuropharmacology · 2015Article
- NMDA-type glutamate receptors participate in reduction of food intake following hindbrain melanocortin receptor activation.American journal of physiology. Regulatory, integrative and comparative physiology · 2015Article
- Role of CA2+/calmodulin on ethanol neurobehavioral effects.Psychopharmacology · 2014Article
- Experimental traumatic brain injury alters ethanol consumption and sensitivity.Journal of neurotrauma · 2014Article
- Adenylyl cylases 1 and 8 mediate select striatal-dependent behaviors and sensitivity to ethanol stimulation in the adolescent period following acute neonatal ethanol exposure.Behavioural brain research · 2014Article
- Postnatal ethanol exposure simplifies the dendritic morphology of medium spiny neurons independently of adenylyl cyclase 1 and 8 activity in mice.Alcoholism, clinical and experimental research · 2014Article
- Soluble adenylyl cyclase activity is necessary for retinal ganglion cell survival and axon growth.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- Ethanol alters endosomal recycling of human dopamine transporters.The Journal of biological chemistry · 2010Article
- The genetics of behavioral alcohol responses in Drosophila.International review of neurobiology · 2010Review
- Region-specific disruption of synapsin phosphorylation following ethanol administration in brain-injured mice.Brain circulationArticle
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
backgroundAlthough ethanol exerts widespread action in the brain, only recently has progress been made in understanding the specific events occurring at the synapse during ethanol exposure. Mice deficient in the calcium-stimulated adenylyl cyclases, AC1 and AC8 (DKO), demonstrate increased sedation duration and impaired phosphorylation by protein kinase A (PKA) following acute ethanol treatment. While not direct targets for ethanol, we hypothesize that these cyclases initiate a homeostatic presynaptic response by PKA to reactivate neurons from ethanol-mediated inhibition. METHODOLOGY/PRINCIPAL
findingsHere, we have used phosphoproteomic techniques and identified several presynaptic proteins that are phosphorylated in the brains of wild type mice (WT) after ethanol exposure, including synapsin, a known PKA target. Phosphorylation of synapsins I and II, as well as phosphorylation of non-PKA targets, such as, eukaryotic elongation factor-2 (eEF-2) and dynamin is significantly impaired in the brains of DKO mice. This deficit is primarily driven by AC1, as AC1-deficient, but not AC8-deficient mice also demonstrate significant reductions in phosphorylation of synapsin and eEF-2 in cortical and hippocampal tissues. DKO mice have a reduced pool of functional recycling vesicles and fewer active terminals as measured by FM1-43 uptake compared to WT controls, which may be a contributing factor to the impaired presynaptic response to ethanol treatment. CONCLUSIONS/SIGNIFICANCE: These data demonstrate that calcium-stimulated AC-dependent PKA activation in the presynaptic terminal, primarily driven by AC1, is a critical event in the reactivation of neurons following ethanol-induced activity blockade.
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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.