Chronic Prenatal Ethanol Exposure Alters Ionotropic Glutamate Receptor Subunit Protein Levels in the Adult Guinea Pig Cerebral Cortex

Dettmer, Todd; Barnes, Alicia; Iqbal, Umar; Bailey, Craig D. C.; Reynolds, James N.; Brien, James F.; Valenzuela, C. Fernando

doi:10.1111/j.1530-0277.2003.tb04404.x

Cited by 22 publications

(9 citation statements)

References 22 publications

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“…These adaptations can lead to prolonged or permanent changes in the structure and function of neurons. There is growing evidence that CET causes alterations in NMDAR subunit levels and composition (Chen et al, 1999;Dettmer et al, 2003;Kalluri et al, 1998;Kumari and Ticku, 2000;Snell et al, 1996;Thomas et al, 1998;Trevisan et al, 1994;Winkler et al, 1999) that could lead to changes in synaptic transmission at glutamatergic synapses. We previously reported that prolonged ethanol caused an increased sensitivity of postsynaptic NMDARs and of presynaptic glutamate release to acute ethanol in CeA (Roberto et al, 2004b).…”

Section: Discussionmentioning

confidence: 99%

Chronic Ethanol Exposure and Protracted Abstinence Alter NMDA Receptors in Central Amygdala

Roberto

Bajo

Crawford

et al. 2005

Neuropsychopharmacol

108

115

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We recently reported that chronic ethanol treatment (CET) and early withdrawal (2-8 h) altered glutamatergic transmission at both preand postsynaptic sites in central nucleus of the amygdala (CeA). Acute ethanol (44 mM) inhibited the NMDA receptor (NMDAR)-mediated EPSCs (NMDA-EPSCs) more in CeA neurons from CET rats than from naïve rats and also decreased paired-pulse facilitation (PPF) of NMDA-EPSCs only in CET rats. To determine whether these CET effects persisted after prolonged withdrawal, we recorded intracellularly in rat CeA slices and measured mRNA and protein expression of CeA NMDAR subunits from CET rats and those withdrawn from ethanol for 1 or 2 weeks. At 1 week withdrawal, acute ethanol decreased evoked NMDA-EPSC amplitudes and NMDA currents induced by exogenous NMDA (B20%) equally to that in naïve rats, indicating that CET effects on postsynaptic mechanisms reversed 1 week after CET cessation. However, acute ethanol still decreased PPF of NMDA-EPSCs, indicating that the acute ethanolinduced increase in glutamate release in CeA seen in CET rats was still present at this time. CET also significantly increased mRNA levels of NR1 and NR2B NMDAR subunits compared to control rats. At 1 week withdrawal, mRNA levels for NR1 and NR2B subunits were significantly decreased. These changes reversed at 2 weeks withdrawal. In Western blots, a significant increase in protein for all three subunits occurred in CeA from CET rats, but not after 1 and 2 weeks of withdrawal. These data indicate that CET induces reversible neuroadaptations in synaptic function, gene expression, and protein composition of NMDAR at CeA synapses. Neuropsychopharmacology (2006) 31, 988-996.

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Section: Discussionmentioning

confidence: 99%

Chronic Ethanol Exposure and Protracted Abstinence Alter NMDA Receptors in Central Amygdala

Roberto

Bajo

Crawford

et al. 2005

Neuropsychopharmacol

108

115

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“…1A, 820 ± 55, 388 ± 44, and 242 ± 32 % of control, respectively) without affecting cAMP levels in these cultures. EHNA accentuated the effect of NMDA on cGMP in DIV 8,13, and 21 cultures (Fig. 1A, 5651 ± 343, 2035 ± 154, and 1152 ± 140 % of control, respectively).…”

Section: Resultsmentioning

confidence: 86%

“…Effect of NMDA receptor activity and PDE activity on cAMP and cGMP levels in maturing primary cortical neuronal cultures Acutely treating primary cortical neuronal cultures with NMDA (30 μM; 15 min) increased cGMP in DIV 8,13, and 21 cultures (Fig. 1A, 744 ± 55, 332 ± 50, and 255 ± 32 % of control, respectively).…”

Section: Resultsmentioning

confidence: 95%

“…Acute treatment with NMDA (30 μM), bicuculline (30 μM), or rolipram (Rol) alone had no effect on cAMP levels in DIV 8,13, and 21 cultures (Fig 1B). However, NMDA or bicuculline in the presence of rolipram (20 μM; 25 min) increased cAMP levels 4-fold in DIV 13 and 21, but had no effect in DIV 8 cultures (Fig.…”

Section: Resultsmentioning

confidence: 98%

“…Band density was quantified using BioRad Quantity One software and reported as arbitrary units, which were converted to percentage of control values from DIV 13 (C) and DIV 21 (D). PDE4A1 and PDE4A5 were immunoprecipitated and their activity was calculated for using PDE activity assay for DIV 13 Primary cortical neuronal cultures were treated starting at DIV 8 for five days with a daily dose of MK-801 (10 μM), MK-801 and dbr-cAMP (500 μM), or MK-801 with dbr-cAMP and BrcGMP (1 mM) and harvested at DIV 13 for SDS-PAGE analysis of PDE4A1, PDE4A5, and actin expression (A). Band density was quantified using BioRad Quantity One software and reported as arbitrary units, which we then converted to percentage of control values (B).…”

Section: Discussionmentioning

confidence: 99%

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Changes in NMDA receptor-induced cyclic nucleotide synthesis regulate the age-dependent increase in PDE4A expression in primary cortical cultures

et al. 2007

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NMDA receptor-induced cAMP and cGMP are selectively hydrolyzed by PDE4 and PDE2, respectively, in rat primary cerebral cortical and hippocampal cultures. Because cAMP levels regulate the expression of PDE4 in rat primary cortical cultures, we examined the manner in which NMDA receptor activity regulates the age-dependent increase in the expression of PDE4A observed in vivo and in vitro. Inhibiting the activity of NR2B subunit with ifenprodil blocked NMDA receptorinduced cGMP synthesis and increased NMDA receptor-induced cAMP levels in a manner that reduced PDE4 activity. Therefore, NR1/NR2B receptor-induced cGMP signaling is involved in an acute cross-talk regulation of NR1/NR2A receptor-induced cAMP levels, mediated by PDE4. Chronic inhibition of NMDA receptor activity with MK-801 reduced PDE4A1 and PDE4A5 expression and activity in a time-dependent manner; this effect was reversed by adding the PKA activator dbr-cAMP. Inhibiting GABA receptors with bicuculline increased NMDA receptorinduced cAMP synthesis and PDE4A expression in cultures treated between DIV 16 and DIV 21 but not in cultures treated between DIV 8 and DIV 13. This effect was due to a high tone of NMDA receptor-induced cGMP in younger cultures, which negatively regulated the expression of PDE4A by a PKG-mediated process. The present results are consistent with behavioral data showing that both PDE4 and PDE2 are involved in NMDA receptor-mediated memory processes.

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Direct and Indirect Mechanisms of Alcohol Teratogenesis: Implications for Understanding Alterations in Brain and Behavior in FASD

Uban

Bodnar

Butts

et al. 2010

Fetal Alcohol Spectrum Disorder

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Chronic Prenatal Ethanol Exposure Alters Ionotropic Glutamate Receptor Subunit Protein Levels in the Adult Guinea Pig Cerebral Cortex

Abstract: These results demonstrate that chronic prenatal ethanol exposure produces long-lasting effects on the subunit composition of NMDA and AMPA receptors in the cerebral cortex of the adult guinea pig.

Cited by 22 publications

References 22 publications

Chronic Ethanol Exposure and Protracted Abstinence Alter NMDA Receptors in Central Amygdala

Chronic Ethanol Exposure and Protracted Abstinence Alter NMDA Receptors in Central Amygdala

Changes in NMDA receptor-induced cyclic nucleotide synthesis regulate the age-dependent increase in PDE4A expression in primary cortical cultures

Direct and Indirect Mechanisms of Alcohol Teratogenesis: Implications for Understanding Alterations in Brain and Behavior in FASD

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