Effect of prenatal alcohol exposure on midsagittal commissure size in rats

Livy, Daniel J.; Elberger, Andrea J.

doi:10.1002/1096-9926(200101)63:1<15::aid-tera1003>3.0.co;2-q

Cited by 16 publications

(13 citation statements)

References 47 publications

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“…It should be noted that the midsagittal area of the rat corpus callosum does not appear to be affected by similar parameters of alcohol exposure (Livy and Elberger, 2001). Therefore, although the results presented here demonstrate an effect of alcohol on the CCpn, these effects are not profound enough to affect severely the overall production of CCpn or their commissural fibres.…”

Section: Discussionmentioning

confidence: 99%

“…Although animal models of fetal alcohol exposure have demonstrated few gross morphological abnormalities in CC structure (Wainwright and Fritz, 1985;Zimmerberg and Scalzi, 1989;Zimmerberg and Mickus, 1990;Livy and Elberger, 2001), the cytoarchitecture of the CCpn has been found to be affected. For example, Miller (1997) found that the density and laminar distribution of CCpn was altered in the somatosensory cortex of ethanol-exposed rats.…”

Section: Introductionmentioning

confidence: 99%

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Alcohol exposure during the first two trimesters-equivalent alters the development of corpus callosum projection neurons in the rat

Livy

Elberger

2008

Alcohol

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Children exposed prenatally to alcohol can display a variety of neural deficits, including an altered development of the corpus callosum (CC), the largest interhemispheric axon pathway in the brain. Furthermore, these children show functional abnormalities that are related to brain regions with significant numbers of CC connections. Little is known about how alcohol imparts influence on CC development, but one possible mechanism is by affecting the corpus callosum projection neurons (CCpn) directly. The purpose of this study was to quantify the effects of prenatal alcohol exposure on the number, size and distribution of CCpn within the visual cortex. The visual cortex was selected specifically due to the many vision-related deficits noted in fetal alcohol exposed children and because the critical role of the CC in visual cortex development is well documented. Sprague-Dawley rat pups received one of four alcohol dosages during gestational days (G) 1-20, or reared as nutritional or untreated control animals. Each litter was categorized according to the peak blood alcohol concentration (BAC) experienced. Pups were removed from each litter on days equivalent to G29, G36, G43, and G50, for histology and measurement. Callosal axons were labelled retrogradely to their CCpn using DiI and the CCpn were then examined using confocal laser scanning microscopy. Differences between alcohol-exposed and control animals were observed in CCpn cell body size, number, and location with the cortex. This was particularly true of animals exposed to high doses of alcohol. In addition, some trends of CCpn development were found to be unchanged as a result of prenatal alcohol exposure. The results demonstrate clear differences in the development of CCpn in the visual cortex between alcohol-exposed and control animals and suggest that this development is particularly affected in those animals exposed to high doses of alcohol.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Alcohol exposure during the first two trimesters-equivalent alters the development of corpus callosum projection neurons in the rat

Livy

Elberger

2008

Alcohol

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“…For example, magnetic resonance imaging studies show that human patients with fetal alcohol syndrome display numerous brain abnormalities, including agenesis of the CC and HC (Bhatara et al, 2002). Rat studies have found that alcohol ingestion during pregnancy can reduce HC size (Livy and Elberger, 2001). Also, reduced CC size in children may be correlated with attention-deficit hyperactivity disorder (ADHD) and dyslexia (Hynd et al, 1991(Hynd et al, , 1995Baumgardner et al, 1996).…”

Section: Discussionmentioning

confidence: 99%

Selective Modification of Short-Term Hippocampal Synaptic Plasticity and Impaired Memory Extinction in Mice with a Congenitally Reduced Hippocampal Commissure

Schimanski¹,

Wahłsten

Nguyen

2002

J. Neurosci.

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The hippocampus is critical for forming new long-term memories, but the contributions of the hippocampal commissure (HC) to memory function and hippocampal synaptic plasticity are unclear. To shed light on this issue, we characterized behavioral memory and hippocampal synaptic plasticity in two inbred mouse strains. BALB/cWah1 mice display a range of corpus callosal defects and an intact HC, whereas 9XCA/Wah mice exhibit a complete absence of corpus callosum and a greatly reduced HC. No differences between strains were found in long-term potentiation (LTP) within two synaptic pathways in hippocampal slices. However, paired-pulse facilitation was deficient in area CA1 of slices from 9XCA/Wah, and it was rescued by decreasing extracellular [Ca 2ϩ ], suggesting that presynaptic calcium dynamics may be altered in this strain. In addition, contextual fear extinction was impaired in 9XCA/Wah mice, but performance on cued fear extinction and on 24 hr memory tests for cued and contextual fear conditioning were not significantly different between strains. Thus, an intact HC is critical for normal extinction of contextual fear. Intact interhemispheric connectivity is not required for acquisition or expression of cued and contextual fear conditioning. LTP was normal in slices from mice that lacked an intact HC, and this was correlated with normal performance on fear conditioning tests. In contrast, impaired short-term synaptic plasticity was correlated with defective contextual memory extinction in mice lacking an intact HC. Thus, the HC in mice is vital for particular aspects of memory function and for short-term synaptic modification in specific hippocampal circuits. Key words: hippocampal commissure; memory; learning; LTP; fear conditioning; extinction; agenesis; mouse strains; synaptic plasticityThe classic case study of H.M., a patient with surgical transection of the medial temporal lobes, demonstrated that the hippocampus is critical for the formation of new declarative memories (Scoville and Milner, 1957). Studies of human commissurotomy patients indicate that the main interhemispheric communication pathway between hippocampi, the hippocampal commissure (HC), is important for normal memory function. Indeed, patients with a transected HC show greater recognition memory deficits than those with an intact HC (Phelps et al., 1991). Patients with transection of both the corpus callosum (CC) and the HC also showed poor memory performance (Zaidel and Sperry, 1974). These findings indicate that an intact CC and HC are required for normal memory function.In two common inbred mouse strains, BALB/c and 129, agenesis of the CC occurs in Ͻ50% of these mice, whereas the remainder appear to have normal forebrain commissures (see Fig.

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“…While gross structural anomalies are usually believed to arise from a disruptive influence during early embryogenesis, Livy and Elberger [88] exposed rats in utero to daily doses of ethanol throughout gestation (equivalent to the first and second trimesters of human gestation) and found that it had no effect on the dimensions of the corpus callosum, although it did reduce the size of a related structure, the hippocampal commissure. Archibald et al [86] reported neuroimaging evidence that both the parietal cortex and the corpus callosum are reduced in size in FASD patients, and we have been able to reproduce this finding by administering a single dose of alcohol to infant mice when they are at an age equivalent to a third trimester human fetus.…”

Section: Can Alcohol Apoptogenicity Explain Signs and Symptoms Of mentioning

confidence: 99%

Drug-Induced Apoptosis: Mechanism by which Alcohol and Many Other Drugs Can Disrupt Brain Development

Creeley

Olney

2013

Brain Sciences

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Maternal ingestion of alcohol during pregnancy can cause a disability syndrome termed Fetal Alcohol Spectrum Disorder (FASD), which may include craniofacial malformations, structural pathology in the brain, and a variety of long-term neuropsychiatric disturbances. There is compelling evidence that exposure to alcohol during early embryogenesis (4th week of gestation) can cause excessive death of cell populations that are essential for normal development of the face and brain. While this can explain craniofacial malformations and certain structural brain anomalies that sometimes accompany FASD, in many cases these features are absent, and the FASD syndrome manifests primarily as neurobehavioral disorders. It is not clear from the literature how alcohol causes these latter manifestations. In this review we will describe a growing body of evidence documenting that alcohol triggers widespread apoptotic death of neurons and oligodendroglia (OLs) in the developing brain when administered to animals, including non-human primates, during a period equivalent to the human third trimester of gestation. This cell death reaction is associated with brain changes, including overall or regional reductions in brain mass, and long-term neurobehavioral disturbances. We will also review evidence that many drugs used in pediatric and obstetric medicine, including general anesthetics (GAs) and anti-epileptics (AEDs), mimic alcohol in triggering widespread apoptotic death of neurons and OLs in the third trimester-equivalent animal brain, and that human children exposed to GAs during early infancy, or to AEDs during the third trimester of gestation, have a significantly increased incidence of FASD-like neurobehavioral disturbances. These findings provide evidence that exposure of the developing human brain to GAs in early infancy, or to alcohol or AEDs in late gestation, can cause FASD-like neurodevelopmental disability syndromes. We propose that the mechanism by which alcohol, GAs and AEDs produce neurobehavioral deficit syndromes is by triggering apoptotic death and deletion of neurons and OLs (or their precursors) from the developing brain. Therefore, there is a need for research aimed at deciphering mechanisms by which these agents trip the apoptosis trigger, the ultimate goal being to learn how to prevent these agents from causing neurodevelopmental disabilities.

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Effect of prenatal alcohol exposure on midsagittal commissure size in rats

Cited by 16 publications

References 47 publications

Alcohol exposure during the first two trimesters-equivalent alters the development of corpus callosum projection neurons in the rat

Alcohol exposure during the first two trimesters-equivalent alters the development of corpus callosum projection neurons in the rat

Selective Modification of Short-Term Hippocampal Synaptic Plasticity and Impaired Memory Extinction in Mice with a Congenitally Reduced Hippocampal Commissure

Drug-Induced Apoptosis: Mechanism by which Alcohol and Many Other Drugs Can Disrupt Brain Development

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