Adverse effects of maternal ethanol consumption on development of dorsal hippocampus in rat offspring

Sakata‐Haga, Hiromi; Sawada, Kazuhiko; Ohta, Kyoko; Cui, Chun; Hisano, Setsuji; Fukui, Yoshihiro

doi:10.1007/s00401-002-0606-9

Cited by 18 publications

(8 citation statements)

References 33 publications

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“…A number of studies have demonstrated that ethanol exposure can induce neuronal circuit abnormalities in the CA3 hippocampal subfield, a region that has been implicated in the pathophysiology of learning and memory alterations associated with FASD (Berman and Hannigan, 2000; Farr et al, 1988; Livy et al, 2003; Maier and West, 2001; Sakata-Haga et al, 2003). It is possible that the inhibitory effects of ethanol exposure on L-type voltage-gated Ca 2+ channel function could contribute to these abnormalities, even if these are only transient, via alterations in Ca 2+ -dependent processes such as gene transcription, protein synthesis, and receptor trafficking, all of which can impact development and refinement of neuronal circuits (Greer and Greenberg, 2008).…”

Section: Discussionmentioning

confidence: 99%

Further characterization of the effect of ethanol on voltage-gated Ca2+ channel function in developing CA3 hippocampal pyramidal neurons

Morton

Valenzuela

2016

Brain Research

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Developmental ethanol exposure damages the hippocampus, a brain region involved in learning and memory. Alterations in synaptic transmission and plasticity may play a role in this effect of ethanol. We previously reported that acute and repeated exposure to ethanol during the 3rd trimester-equivalent inhibits long-term potentiation of GABAA receptor-dependent synaptic currents in CA3 pyramidal neurons through a mechanism that depends on retrograde release of brain-derived neurotrophic factor driven by activation of voltage-gated Ca2+ channels (Zucca and Valenzuela, 2010). We found evidence indicating that voltage-gated Ca2+ channels are inhibited in the presence of ethanol, an effect that may play a role in its mechanism of action. Here, we further investigated the acute effect of ethanol on the function of voltage-gated Ca2+ channels in CA3 pyramidal neurons using Ca2+ imaging techniques. These experiments revealed that acute ethanol exposure inhibits voltage-gated Ca2+ channels both in somatic and proximal dendritic compartments. To investigate the long-term consequences of ethanol on voltage-gated Ca2+ channels, we used patch-clamp electrophysiological techniques to assess the function of L-type voltage-gated Ca2+ channels during and following ten days of vapor ethanol exposure. During ethanol withdrawal periods, the function of these channels was not significantly affected by vapor chamber exposure. Taken together with our previous findings, our results suggest that 3rd trimester-equivalent ethanol exposure transiently inhibits L-type voltage-gated Ca2+ channel function in CA3 pyramidal neurons and that compensatory mechanisms restore their function during ethanol withdrawal. Transient inhibition of these channels by ethanol may be, in part, responsible for the hippocampal abnormalities associated with developmental exposure to this agent.

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Section: Discussionmentioning

confidence: 99%

Further characterization of the effect of ethanol on voltage-gated Ca2+ channel function in developing CA3 hippocampal pyramidal neurons

Morton

Valenzuela

2016

Brain Research

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“…Several studies have shown the importance of neural cell adhesion molecules in the normal brain development and that alcohol alters the expression of these molecules during neurogenesis (Miller and Luo, 2002; Miller et al., 2006; Minana et al., 2000; Nagy et al., 2002; Sakata‐Haga et al., 2003; Siegenthaler and Miller, 2004). We suggest that ETOH‐induced changes in cell adhesion molecule expression may underlie the observed accelerated coalescence of neurospheres in vitro .…”

Section: Discussionmentioning

confidence: 99%

Ethanol Increases Fetal Human Neurosphere Size and Alters Adhesion Molecule Gene Expression

Vangipuram

Grever

Parker

et al. 2007

Alcoholism Clin & Exp Res

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“…This includes significant loss of pyramidal neurons in CA1 and CA3 and granule neurons in the dentate gyrus (Ieraci & Herrera, 2007; Ikonomidou et al, 2000; Klintsova et al, 2007; Livy, Miller, Maier, & West, 2003; Tran & Kelly, 2003; Uban et al, 2010). Developmental ethanol exposure also produces neuroanatomical and electrophysiological defects in hippocampal circuitry (Diaz et al, 2014; Everett, Licon-Munoz, & Valenzuela, 2012; Lindquist, Sokoloff, Milner, & Steinmetz, 2013; Sakata-Haga et al, 2003). Defects in the hippocampus correlate with behavioral deficits, particularly with learning and memory (Banuelos et al, 2012; El Shawa et al, 2013; Hamilton et al, 2010; Idrus, McGough, Riley, & Thomas, 2014; Kelly, Pierce, & West, 1987; Thomas, Idrus, Monk, & Dominguez, 2010; Wagner, Zhou, & Goodlett, 2014; West, Kelly, & Pierce, 1987; Zink et al, 2011).…”

Section: Fasd Neuropathology In Animal Modelsmentioning

confidence: 99%

Fetal Alcohol Spectrum Disorders and Neuroimmune Changes

Drew

Kane

2014

International Review of Neurobiology

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The behavioral consequences of fetal alcohol spectrum disorders (FASD) are serious and persist throughout life. The causative mechanisms underlying FASD are poorly understood. However, much has been learned about FASD from human structural and functional studies as well as from animal models, which have provided a greater understanding of the mechanisms underlying FASD. Using animal models of FASD, it has been recently discovered that ethanol induces neuroimmune activation in the developing brain. The resulting microglial activation, production of proinflammatory molecules, and alteration in expression of developmental genes are postulated to alter neuron survival and function and lead to long-term neuropathological and cognitive defects. It has also been discovered that microglial loss occurs, reducing microglia’s ability to protect neurons and contribute to neuronal development. This is important, because emerging evidence demonstrates that microglial depletion during brain development leads to long-term neuropathological and cognitive defects. Interestingly, the behavioral consequences of microglial depletion and neuroimmune activation in the fetal brain are particularly relevant to FASD. This chapter reviews the neuropathological and behavioral abnormalities of FASD and delineates correlates in animal models. This serves as a foundation to discuss the role of the neuroimmune system in normal brain development, the consequences of microglial depletion and neuroinflammation, the evidence of ethanol induction of neuroinflammatory processes in animal models of FASD, and the development of anti-inflammatory therapies as a new strategy for prevention or treatment of FASD. Together, this knowledge provides a framework for discussion and further investigation of the role of neuroimmune processes in FASD.

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Adverse effects of maternal ethanol consumption on development of dorsal hippocampus in rat offspring

Cited by 18 publications

References 33 publications

Further characterization of the effect of ethanol on voltage-gated Ca2+ channel function in developing CA3 hippocampal pyramidal neurons

Further characterization of the effect of ethanol on voltage-gated Ca2+ channel function in developing CA3 hippocampal pyramidal neurons

Ethanol Increases Fetal Human Neurosphere Size and Alters Adhesion Molecule Gene Expression

Fetal Alcohol Spectrum Disorders and Neuroimmune Changes

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