Effects of prenatal alcohol exposure on brain-derived neurotrophic factor and its receptor tyrosine kinase B in offspring

Feng, Ming; Yan, Shu-E; Yan, Qing‐Shan

doi:10.1016/j.brainres.2005.02.017

Cited by 62 publications

(53 citation statements)

References 30 publications

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“…Although we cannot definitely distinguish between the two, the observed reduction in frequency further supports the idea that ethanol inhibits glutamate release in the CA1 hippocampal region (Mameli et al, 2005;Hendricson et al, 2003;Maldve et al, 2004). In addition, prenatal ethanol exposure has been shown to reduce levels of BDNF protein and mRNA levels in the hippocampus (Feng et al, 2005), which can influence AMPA and NMDA receptor-mediated synaptic transmission (Aicardi et al, 2004;Kossel et al, 2001;Kang et al, 1997;Abidin et al, 2006;Rex et al, 2006). However, at present, there are no reports available to our knowledge regarding the influence of prenatal alcohol exposure on the BDNF levels in offspring of the age group used in this study.…”

Section: Therapeutic Effects Of Aniracetamsupporting

confidence: 54%

“…However, at present, there are no reports available to our knowledge regarding the influence of prenatal alcohol exposure on the BDNF levels in offspring of the age group used in this study. Therefore, as suggested by Feng et al (2005), it is reasonable to presume that in utero ethanol-induced reduction of BDNF protein and mRNA expression might play a role in the decreasing amplitude and frequency of AMPAR-mediated mEPSCs.…”

Section: Therapeutic Effects Of Aniracetammentioning

confidence: 97%

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Aniracetam Reversed Learning and Memory Deficits Following Prenatal Ethanol Exposure by Modulating Functions of Synaptic AMPA Receptors

Vaglenova

Pandiella

Wijayawardhane

et al. 2007

Neuropsychopharmacol

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Specific pharmacological treatments are currently not available to address problems resulting from fetal ethanol exposure, described as Fetal Alcohol Syndrome or Fetal Alcohol Spectrum Disorders (FASD). The present study evaluated the therapeutic effects of aniracetam against cognitive deficits in a well-characterized and sensitive FASD Sprague-Dawley rat model. Ethanol, administered orally at a moderate dose (4 g/kg/24 h; 38% v/v) during the entire course of pregnancy, caused severe cognitive deficits in offspring. Furthermore, both progeny genders were affected by a spectrum of behavioral abnormalities, such as a delay in the development of the righting reflex, poor novelty seeking behavior, and high anxiety levels in female rats. Cognitive disabilities, monitored in adult rats by a two-way active avoidance task, correlated well with a significant reduction of AMPA (a-amino-3 hydro-5 methyl-isoxazole propionic acid) receptormediated miniature excitatory postsynaptic responses (mEPSCs) in the hippocampus. Administration of aniracetam for 10 days (postnatal days (PND) 18-27), at a dose of 50 mg/kg reversed cognitive deficits in both rat genders, indicated by a significant increase in the number of avoidances and the number of 'good learners'. After the termination of the nootropic treatment, a significant increase in both amplitude and frequency of AMPA receptor-mediated mEPSCs in hippocampal CA-1 pyramidal cells was observed. Significant anxiolytic effects on PND 40 also preceded acquisition improvements in the avoidance task. This study provides evidence for the therapeutic potential of aniracetam in reversing cognitive deficits associated with FASD through positive post-natal modulation of AMPA receptors.

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Section: Therapeutic Effects Of Aniracetamsupporting

confidence: 54%

Section: Therapeutic Effects Of Aniracetammentioning

confidence: 97%

Aniracetam Reversed Learning and Memory Deficits Following Prenatal Ethanol Exposure by Modulating Functions of Synaptic AMPA Receptors

Vaglenova

Pandiella

Wijayawardhane

et al. 2007

Neuropsychopharmacol

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“…Animals exposed prenatally to ethanol have decreased TrkB phosphorylation at 1 week of age that is probably secondary to a decrease in BDNF (Climent et al, 2002;Feng et al, 2005;Fattori et al, 2008). Chronic ethanol exposure increases ERK activity in cultured cortical neurons and pheochromocytoma cells (Kalluri and Ticku, 2003;Roivainen et al, 1995) while acute ethanol administration decreases activation of ERK (Chandler and Sutton, 2005;Han et al, 2006;Kalluri and Ticku, 2002;Kalluri and Ticku 2003;Tsuji et al, 2003;Fattori et al, 2008;Ohrtman et al, 2006, however, see Acquaah-Mensah et al, 2001).…”

Section: Effects Of Etoh On Bdnf Signalingmentioning

confidence: 99%

“…The discrepancy in these data is not likely due to timing of exposure since conflicting results were also obtained with gestational exposure, but may be due age of the animals at analysis. Heatonet al (2000) measured levels at PN1, while Feng et al (2005) examined BDNF levels at PN7 and Climent et al (2002) measured levels at PN5, PN14, PN21 and PN35 after gestational exposure.…”

Section: Is Bdnf Involved In Fasd?mentioning

confidence: 99%

“…Examination of BDNF signaling (discussed below) suggests that ethanol causes a decrease in the ability of TrkB to transduce signal and desensitize, which may lead to compensatory regulation of both BDNF and TrkB in vivo. The data from Feng et al (2005) and Climent et al (2002) suggest that the end result is a decrease in BDNF during post-exposure development that may be secondary to impaired synaptogenesis and neuronal apoptosis.…”

Section: Is Bdnf Involved In Fasd?mentioning

confidence: 99%

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Ethanol–BDNF interactions: Still more questions than answers

Davis

2008

Pharmacology & Therapeutics

127

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Brain Derived Neurotrophic Factor (BDNF) has emerged as a regulator of development, plasticity and, recently, addiction. Decreased neurotrophic activity may be involved in ethanol-induced neurodegeneration in the adult brain and in the etiology of alcohol-related neurodevelopmental disorders. This can occur through decreased expression of BDNF or through inability of the receptor to transduce signals in the presence of ethanol. In contrast, recent studies implicate region-specific up-regulation of BDNF and associated signaling pathways in anxiety, addiction and homeostasis after ethanol exposure. Anxiety and depression are precipitating factors for substance abuse and these disorders also involve region-specific changes in BDNF in both pathogenesis and response to pharmacotherapy. Polymorphisms in the genes coding for BDNF and its receptor TrkB are linked to affective, substance abuse and appetitive disorders and therefore may play a role in the development of alcoholism. This review summarizes historical and pre-clinical data on BDNF and TrkB as it relates to ethanol toxicity and addiction. Many unresolved questions about region-specific changes in BDNF expression and the precise role of BDNF in neuropsychiatric disorders and addiction remain to be elucidated. Resolution of these questions will require significant integration of the literature on addiction and comorbid psychiatric disorders that contribute to the development of alcoholism.

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Multiple exposures to environmental pollutants and oxidative stress: Is there a sex specific risk of developmental complications for fetuses?

Al-Gubory

2016

Birth Defects Research Pt C

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Medically assisted procreation significantly contributes to an increase in twin pregnancies. One of the major factors contributing to more twin births is the use of fertility treatments. Twin pregnancy is not without a risk for fetal organ development and the health outcome of new‐borns, children, and adults. Multiple pregnancies are associated with an increased risk of developmental complications, such as perinatal mortality, premature births, and low birth weight. Oxidative stress is involved in pregnancy disorders such as abortion, intrauterine growth retardation, and prenatal mortality. The link between oxidative stress and prenatal development, poorly perceived in the medical community, is a major problem in human reproductive medicine and health outcomes. The sex‐based considerations and analyses are also, often neglected in biomedical research. In addition, fetal sexual dimorphism in antioxidant pathways following intrauterine exposure to environmental pollutants has not been explored. This is an important area of research because sexually dimorphic antioxidant adaptive responses to early life exposure‐induced oxidative stress may have long‐term effects on offspring health outcome and increase the risk of non‐communicable diseases in men and women. This concept is useful, since it may open the avenue to develop antenatal antioxidant therapeutic strategies to developmental disorders and complications related to multiple pregnancies, and in association with acute or chronic environmental exposure. This article reviews the status of research, supporting data, possible pathogenic mechanisms, and future perspectives in the proposed area. Birth Defects Research (Part C) 108:351–364, 2016. © 2016 Wiley Periodicals, Inc.

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Effects of prenatal alcohol exposure on brain-derived neurotrophic factor and its receptor tyrosine kinase B in offspring

Cited by 62 publications

References 30 publications

Aniracetam Reversed Learning and Memory Deficits Following Prenatal Ethanol Exposure by Modulating Functions of Synaptic AMPA Receptors

Aniracetam Reversed Learning and Memory Deficits Following Prenatal Ethanol Exposure by Modulating Functions of Synaptic AMPA Receptors

Ethanol–BDNF interactions: Still more questions than answers

Multiple exposures to environmental pollutants and oxidative stress: Is there a sex specific risk of developmental complications for fetuses?

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