Administration of eliprodil during ethanol withdrawal in the neonatal rat attenuates ethanol-induced learning deficits

Thomas, Jennifer D.; Garcia, Gabriela; Dominguez, Hector D.; Riley, Edward P.

doi:10.1007/s00213-004-1806-x

Cited by 41 publications

(60 citation statements)

References 41 publications

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“…PNEE increases fetal levels of glutamate (Karl et al, 1995) and administration of an NMDAR antagonist following PNEE can rescue ethanol-induced deficits in offspring spatial memory (Thomas et al, 2004). These studies suggest that heightened NMDAR activity due to ethanol-induced increases in glutamate might also contribute to ethanol toxicity.…”

Section: Discussionmentioning

confidence: 97%

Prenatal ethanol exposure enhances NMDAR‐dependent long‐term potentiation in the adolescent female dentate gyrus

Titterness

Christie

2010

Hippocampus

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The dentate gyrus (DG) is a region of the hippocampus intimately involved with learning and memory. Prenatal exposure to either stress or ethanol can reduce long-term potentiation (LTP) in the male hippocampus but there is little information on how these prenatal events affect LTP in the adolescent female hippocampus. Previous studies suggest that deleterious effects of PNEE can, in part, be mediated by corticosterone, suggesting that prenatal stress might further enhance any alterations to LTP induced PNEE. When animals were exposed to a combination of prenatal stress and PNEE distinct sex differences emerged. Exposure to ethanol throughout gestation significantly reduced DG LTP in adolescent males but enhanced LTP in adolescent females. Combined exposure to stress and ethanol in utero reduced the ethanol-induced enhancement of LTP in females. On the other hand, exposure to stress and ethanol in utero did not alter the ethanol-induced reduction of LTP in males. These results indicate that prenatal ethanol and prenatal stress produce sex-specific alterations in synaptic plasticity in the adolescent hippocampus.

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Section: Discussionmentioning

confidence: 97%

Prenatal ethanol exposure enhances NMDAR‐dependent long‐term potentiation in the adolescent female dentate gyrus

Titterness

Christie

2010

Hippocampus

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“…Given the wide range of actions of agmatine throughout the CNS, it is possible that the protection observed in our study was partly based on some of these additional mechanisms, independent of NMDAR modulation. However, additional behavioral work from our laboratory and others (Thomas et al, 2004), using more specific NR2B or polyamine antagonists, as well as cell culture studies specifically examining the effects of agmatine and polyamines on glutamate-induced cell death (Gibson et al, 2003) favor an NMDAR/polyamine modulation hypothesis.…”

Section: Discussionmentioning

confidence: 99%

“…Although the side effects of MK-801 preclude its use clinically, success in animal models of early ethanol exposure has generated interest in alternate NMDAR antagonists that may be more viable. At least three types of antagonists seem particularly promising; low-affinity, non-competitive NMDAR channel blockers such as memantine (Volbracht et al, 2006), which is currently used clinically for treating Alzheimer's disease, NR2B subunit antagonists such as ifenprodil or eliprodil (Nikam & Meltzer, 2002;Thomas et al, 2004), and agents that modulate rather than block NMDAR activity such as agmatine, which can act at the polyamine binding site, resulting in allosteric modulation of the receptor.…”

Section: Introductionmentioning

confidence: 99%

Agmatine reduces balance deficits in a rat model of third trimester binge-like ethanol exposure

Lewis

Wellmann

Barron

2007

Pharmacology Biochemistry and Behavior

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This study examined the effects of binge-like ethanol (ETOH) exposure in neonatal rats on a cerebellar-mediated balance task, and the ability of agmatine, an n-methyl-d-aspartate receptor (NMDAR) modulator, to reverse such effects. Five neonatal treatments groups were used, including ETOH (6.0 g/kg/day), AG (20 mg/kg), ETOH plus AG (6.0 g/kg/day and 20 mg/kg), a maltose control, and a non-treated control. Ethanol was administered via oral intubation twice daily for eight days, (AG was administered with the last ETOH intubation only). Two exposure periods were used; PND 1-8 or PND 8-15. On PND 31-33, balance performance on a single dowel was tested. Treatment with AG during withdrawal in ETOH exposed animals improved performance relative to ETOH alone among the PND 1-8 exposure period. ETOH exposure during the 2 nd postnatal week did not impair balance. These findings provide further support that exposure to ETOH during critical developmental periods can impair performance on a cerebellar-dependent balance task. Of perhaps greater significance, co-administration of agmatine reduced these deficits suggesting that NMDA modulation via polyamine blockade may provide a novel approach to attenuating damage associated with binge-like ETOH consumption.

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“…[4,5]) and/or pharmacological treatments (e.g. [6][7][8]) of FASD and mechanisms of alcohol-induced damage (e.g. [9,10]).…”

Section: Introductionmentioning

confidence: 99%

Intragastric Intubation of Alcohol During the Perinatal Period

Kelly

Lawrence

2008

Methods in Molecular Biology™

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Animal models of fetal alcohol spectrum disorder (FASD) have been instrumental in isolating alcohol as a teratogen and demonstrating behavioral and neural effects. There are a number of different models for rodents with various strengths and weaknesses. A three-trimester model of FASD is described here; the model uses intragastric intubation of both pregnant dams and pups to mimic alcohol exposure across all three trimesters in humans. The model does not use expensive equipment and is relatively easy to accomplish. The model allows excellent control of alcohol dose and uses an oral route of administration. There are no undernutrition effects with the doses used here. A drawback of the model is the stress of the intubation procedures and ways in which to minimize this stress are discussed. In addition, a method to measure blood alcohol levels is described.

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Administration of eliprodil during ethanol withdrawal in the neonatal rat attenuates ethanol-induced learning deficits

Abstract: These data support the hypothesis that NMDA receptor-mediated excitotoxicity during ethanol withdrawal contributes to fetal alcohol effects.

Cited by 41 publications

References 41 publications

Prenatal ethanol exposure enhances NMDAR‐dependent long‐term potentiation in the adolescent female dentate gyrus

Prenatal ethanol exposure enhances NMDAR‐dependent long‐term potentiation in the adolescent female dentate gyrus

Agmatine reduces balance deficits in a rat model of third trimester binge-like ethanol exposure

Intragastric Intubation of Alcohol During the Perinatal Period

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