ArticleAnatomy & cell biology2011
Modulation by the GABA(B) receptor siRNA of ethanol-mediated PKA-α, CaMKII, and p-CREB intracellular signaling in prenatal rat hippocampal neurons.
Article in Anatomy & cell biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed, 11 citations in OpenAlex.
- Konjac Oligosaccharide Alleviates Constipation in Mice via 5-HT4R/cAMP/PKA/p-CREB Pathway Activation.Current medical science · 2025Article
- Inhibition of phosphodiesterase 2 reverses impaired cognition and neuronal remodeling caused by chronic stress.Neurobiology of aging · 2015Article
- Xylaria nigripes mitigates spatial memory impairment induced by rapid eye movement sleep deprivation.International journal of clinical and experimental medicine · 2014Article
- αCaMKII autophosphorylation controls the establishment of alcohol drinking behavior.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2013Article
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Authors and funding
7 authors at 1 institution in 1 country.
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Abstract
Fetal alcohol syndrome (FAS) is a developmental neuropathology resulting from in utero exposure to ethanol; many of ethanol's effects are likely to be mediated by the neurotransmitter γ-aminobutyric acid (GABA). We studied modulation of the neurotransmitter receptor GABA(B)R and its capacity for intracellular signal transduction under conditions of ethanol treatment (ET) and RNA interference to investigate a potential role for GABA signaling in FAS. ET increased GABA(B1)R protein levels, but decreased protein kinase A-α (PKA-α), calcium/calmodulin-dependent protein kinase II (CaMKII) and phosphorylation of cAMP-response element binding protein (p-CREB), in cultured hippocampal neurons harvested at gestation day 17.5. To elucidate GABA(B1)R response to ethanol, we observed the effects of a GABA(B)R agonist and antagonist in pharmacotherapy for ethanol abuse. Baclofen increased GABA(B)R, CaMKII and p-CREB levels, whereas phaclofen decreased GABA(B)R, CaMKII and p-CREB levels except PKA-α. Furthermore, when GABA(B1)R was knocked down by siRNA treatment, CaMKII and p-CREB levels were reduced upon ET. We speculate that stimulation of GABA(B1)R activity by ET can modulate CaMKII and p-CREB signaling to detrimental effect on fetal brain development.
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