Ethanol modulates the expression of GABAB receptor mRNAs in the prenatal rat brain in an age and area dependent manner

Li, S.P.; Kim, J.H.; Park, M.S.; Bahk, Jong Yoon; Chung, Bong Chul; Kim, M.O.

doi:10.1016/j.neuroscience.2005.05.001

Cited by 6 publications

(10 citation statements)

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“…The highest expression of GABA B1 R occurs in GD 17.5 fetuses. The protein level changes could not be attributed to changes in the level of transcription since GABA B1 R mRNA presented different expression patterns upon in vivo ethanol treatment, which were similar to our previous results (Li et al, 2005a). In the present study we further revealed age-dependent differential expression pattern of GABA B2 R than that of the GABA B1 R expression under the same condition, as mentioned above.…”

Section: Discussionsupporting

confidence: 92%

“…The protein level changes could not be attributed to changes in the level of transcription since GABA B1 R mRNA presented different expression patterns, showing an age-dependent increase, with the highest expression levels in GD 19.5, followed by GD 21.5 and 17.5 respectively (Fig. 2), which were similar to our previous results (Li et al, 2005a). To further define the effects of ethanol on GABA B1 R expression, we employed fetuses from different developmental stages treated with maternal ethanol.…”

Section: In Vivo Maternal Ethanol Exposure On Gaba B R Expression In supporting

confidence: 90%

“…For RPAs, we used the RPA II kit (Ambion) unless otherwise specified (Li et al, 2004(Li et al, , 2005a. The gelpurified probes were reconstituted in hybridization buffer to a concentration of 500,000 cpm/20 ll and hybridized to 20 lg (GABA B1 R) of total RNA.…”

Section: Rna Protection Assaymentioning

confidence: 99%

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In vivo and in vitro ethanol exposure in prenatal rat brain: GABA_B receptor modulation on dopamine D₁ receptor and protein kinase A

Lee

Naha

et al. 2008

Synapse

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We have investigated the effects of prenatal ethanol exposure on GABA(B) receptors (GABA(B)Rs), protein kinase A (PKA), and DA D(1) receptor (DAD(1)R) expressions. GABA(B1)R and GABA(B2)R showed different age-dependent expressions in in vivo fetal rat forebrain from gestational days (GD) 15.5 to 21.5 upon 10% ethanol treatment to mother, with and without baclofen at a dose of 10 mg/kg body weight/day. The protein level changes could not be attributed to changes in the level of transcription since GABA(B)R mRNA presented different expression patterns upon in vivo ethanol treatment. Using in vitro cultivated cortical neurons from GD 17.5 fetuses, we also explored the modulatory effects of ethanol on PKA and DAD(1)R through GABA(B)Rs, under 50 microM baclofen and 100 microM phaclofen administrations, with or without 100 mM of ethanol treatment in the culture media. The results showed that 20 min ethanol treatment without baclofen or phaclofen had increasing effects on both the GABA(B)Rs. Further, baclofen and phaclofen administration significantly affected PKA and GABA(B)R levels upon 20 min and 1 h ethanol treatment. In contrast, DAD(1)R showed increasing effects upon ethanol treatment, which was modulated by GABA(B)R's agonist baclofen and antagonist phaclofen. Therefore the present study suggested that the GABA(B)R activity could modulate ethanol's cellular effects, which possibly including PKA and DAD(1)R activities, and may be an underlying cause of ethanol's effects.

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Section: Discussionsupporting

confidence: 92%

Section: In Vivo Maternal Ethanol Exposure On Gaba B R Expression In supporting

confidence: 90%

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In vivo and in vitro ethanol exposure in prenatal rat brain: GABA_B receptor modulation on dopamine D₁ receptor and protein kinase A

Lee

Naha

et al. 2008

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“…We have additionally tested the modulatory effects of a GABA B1 R agonist and/or antagonist on ET-mediated GABA-ergic signaling, as well as that of GABA B1 R gene knockdown. We find that ethanol regulates GABA B R expression disparately at mRNA and protein levels, suggesting that these effects are not completely attributable to changes in gene expression as previously mentioned [21]. …”

Section: Discussionsupporting

confidence: 62%

Modulation by the GABA_Breceptor siRNA of ethanol-mediated PKA-α, CaMKII, and p-CREB intracellular signaling in prenatal rat hippocampal neurons

et al. 2011

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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 GABABR 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 GABAB1R 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 GABAB1R response to ethanol, we observed the effects of a GABABR agonist and antagonist in pharmacotherapy for ethanol abuse. Baclofen increased GABABR, CaMKII and p-CREB levels, whereas phaclofen decreased GABABR, CaMKII and p-CREB levels except PKA-α. Furthermore, when GABAB1R was knocked down by siRNA treatment, CaMKII and p-CREB levels were reduced upon ET. We speculate that stimulation of GABAB1R activity by ET can modulate CaMKII and p-CREB signaling to detrimental effect on fetal brain development.

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“…Most experimental models of prenatal ethanol exposure use chronic intoxication to simulate the outcome of FAS and report several brain abnormalities (Miller,1985,1986,1988,1989,1993,1995a,b,2006; Miller and Potempa,1990; Miller and Nowakowski,1991; Miller and Robertson,1993; Mooney and Miller,2001,2003). Just a few studies use acute or short‐term exposure to address the role of ethanol abuse on specific cell populations (Miller,1996; Obernier et al,2002; Li et al,2005; Mooney and Miller,2007; Oyedele and Kramer,2008).…”

Section: Experimental Models Of Prenatal Ethanol Exposurementioning

confidence: 99%

Impact of Ethanol on the Developing GABAergic System

Isayama

Leite

Lima

et al. 2009

The Anatomical Record

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Alcohol intake during pregnancy has a tremendous impact on the developing brain. Embryonic and early postnatal alcohol exposures have been investigated experimentally to elucidate the fetal alcohol spectrum disorders' (FASD) milieu, and new data have emerged to support a devastating effect on the GABAergic system in the adult and developing nervous system. GABA is a predominantly inhibitory neurotransmitter that during development excites neurons and orchestrates several developmental processes such as proliferation, migration, differentiation, and synaptogenesis. This review summarizes and brings new data on neurodevelopmental aspects of the GABAergic system with FASD in experimental telencephalic models. Anat Rec, 292:1922Rec, 292: -1939Rec, 292: , 2009. Key words: GABA; developing brain; prenatal ethanol exposure; cortical neurons; ganglionic eminence THE DEVELOPING TELENCEPHALONThe central nervous system develops in a programmed order, following subsequent steps. Because of the cellular diversity and complexity throughout its laminar and areal structure, the cerebral cortex is a good model for studying developmental events. After closure of the neural tube, progenitor cells located near its lumen (ventricular zones) start to proliferate intensely, first to increase progenitor pool and then to originate postmitotic cells (Rakic, 1988). The destination of proliferating cells is largely influenced by their mitotic spindle rotation during metaphase and their cleavage plane during Abbreviations used: ARBD ¼ alcohol-related birth defects; ARND ¼ alcohol-related neurodevelopmental disorders; BDNF ¼ brain-derived neurotrophic factor; BrdU ¼ bromodeoxyuridine;

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Ethanol modulates the expression of GABAB receptor mRNAs in the prenatal rat brain in an age and area dependent manner

Cited by 6 publications

References 41 publications

In vivo and in vitro ethanol exposure in prenatal rat brain: GABA_B receptor modulation on dopamine D₁ receptor and protein kinase A

In vivo and in vitro ethanol exposure in prenatal rat brain: GABA_B receptor modulation on dopamine D₁ receptor and protein kinase A

Modulation by the GABA_Breceptor siRNA of ethanol-mediated PKA-α, CaMKII, and p-CREB intracellular signaling in prenatal rat hippocampal neurons

Impact of Ethanol on the Developing GABAergic System

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Ethanol modulates the expression of GABAB receptor mRNAs in the prenatal rat brain in an age and area dependent manner

Cited by 6 publications

References 41 publications

In vivo and in vitro ethanol exposure in prenatal rat brain: GABAB receptor modulation on dopamine D1 receptor and protein kinase A

In vivo and in vitro ethanol exposure in prenatal rat brain: GABAB receptor modulation on dopamine D1 receptor and protein kinase A

Modulation by the GABABreceptor siRNA of ethanol-mediated PKA-α, CaMKII, and p-CREB intracellular signaling in prenatal rat hippocampal neurons

Impact of Ethanol on the Developing GABAergic System

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In vivo and in vitro ethanol exposure in prenatal rat brain: GABA_B receptor modulation on dopamine D₁ receptor and protein kinase A

In vivo and in vitro ethanol exposure in prenatal rat brain: GABA_B receptor modulation on dopamine D₁ receptor and protein kinase A

Modulation by the GABA_Breceptor siRNA of ethanol-mediated PKA-α, CaMKII, and p-CREB intracellular signaling in prenatal rat hippocampal neurons