Effects of early ethanol exposure on dendrite growth of cortical pyramidal neurons: inferences from a computational model

Granato, Alberto; Pelt, Jaap van

doi:10.1016/s0165-3806(03)00094-4

Cited by 33 publications

(21 citation statements)

References 20 publications

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“…The amount of information that a neuron can receive from the environment depends on the number of branch points of dendrites and the size of the dendritic field. Evidences have shown that dendritic morphology may change with the age and the phase of an individual, especially in the early life (Granato and Pelt, 2003).…”

Section: Discussionmentioning

confidence: 99%

Prenatal stress causes dendritic atrophy of pyramidal neurons in hippocampal CA3 region by glutamate in offspring rats

Jia

Yang

Sun

et al. 2009

Developmental Neurobiology

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A substantial number of human epidemiological data, as well as experimental studies, suggest that adverse maternal stress during gestation is involved in abnormal behavior, mental, and cognition disorder in offspring. To explore the effect of prenatal stress (PS) on hippocampal neurons, in this study, we observed the dendritic field of pyramidal neurons in hippocampal CA3, examined the concentration of glutamate (Glu), and detected the expression of synaptotagmin-1 (Syt-1) and N-methyl-D-aspartate receptor 1 (NR1) in hippocampus of juvenile female offspring rats. Pregnant rats were divided into two groups: control group (CON) and PS group. Female offspring rats used were 30-day old. The total length of the apical dendrites of pyramidal neurons in hippocampal CA3 of offspring was significantly shorter in PS than that in CON (p< 0.01). The number of branch points of the apical dendrites of pyramidal neurons in hippocampal CA3 of offspring was significantly less in PS (p < 0.01). PS offspring had a higher concentration of hippocampal Glu compared with CON (p < 0.05). PS offspring displayed increased expression of Syt-1 and decreased NR1 in hippocampus compared with CON (p < 0.001 and p < 0.01, respectively). The expression of NR1 in different hippocampus subfields of offspring was significantly decreased in PS than that in CON (p < 0.05-0.01). This study shows that PS increases the Glu in hippocampus and causes apical dendritic atrophy of pyramidal neurons of hippocampal CA3 in offspring rats. The decline of NR1 in hippocampus may be an adaptive response to the increased Glu.

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Section: Discussionmentioning

confidence: 99%

Prenatal stress causes dendritic atrophy of pyramidal neurons in hippocampal CA3 region by glutamate in offspring rats

Jia

Yang

Sun

et al. 2009

Developmental Neurobiology

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“…Alcohol exposure continues to have potent effect on brain development postnatally in rodents, demonstrated by studies showing dramatic effects on the number of layer 2/3 cortical pyramidal neurons, on the branching patterns of their basilar dendrites Granato and Van Pelt, 2003), and on dendritic excitability . The same group has gone on to also implicate distinct alterations in cerebral cortical and striatal interneuron distribution and morphology Granato, 2006).…”

Section: Alcoholmentioning

confidence: 99%

Developmental Consequences of Fetal Exposure to Drugs: What We Know and What We Still Must Learn

Ross

Graham

Money

et al. 2014

Neuropsychopharmacol

333

241

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Most drugs of abuse easily cross the placenta and can affect fetal brain development. In utero exposures to drugs thus can have long-lasting implications for brain structure and function. These effects on the developing nervous system, before homeostatic regulatory mechanisms are properly calibrated, often differ from their effects on mature systems. In this review, we describe current knowledge on how alcohol, nicotine, cocaine, amphetamine, Ecstasy, and opiates (among other drugs) produce alterations in neurodevelopmental trajectory. We focus both on animal models and available clinical and imaging data from cross-sectional and longitudinal human studies. Early studies of fetal exposures focused on classic teratological methods that are insufficient for revealing more subtle effects that are nevertheless very behaviorally relevant. Modern mechanistic approaches have informed us greatly as to how to potentially ameliorate the induced deficits in brain formation and function, but conclude that better delineation of sensitive periods, dose-response relationships, and long-term longitudinal studies assessing future risk of offspring to exhibit learning disabilities, mental health disorders, and limited neural adaptations are crucial to limit the societal impact of these exposures.

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“…Accordingly, chemicals that affect the process of neurite outgrowth have the potential to cause developmental neurotoxicity. Although it has been shown that neurite outgrowth is vulnerable to chemical insult during development, morphological assessment of this endpoint in vivo is labor-intensive and requires the use of advanced techniques including immunocytochemical staining, dye injection and advanced microscopy (Alfano and Petit, 1982;Granato and Van Pelt, 2003). The in vitro studies cited in this review demonstrate the ability of cell culture models to provide a relatively simple system for monitoring the complex morphological changes which accompany process outgrowth.…”

Section: Discussionmentioning

confidence: 98%

“…Out of the 35 chemicals listed in Table 2, references for changes in axonal or dendritic outgrowth after in vivo exposure were noted for only four. Changes in axonal or dendritic morphology have been observed after developmental exposure to the neurotoxicants lead (Alfano and Petit, 1982;Campbell et al, 1982;Reuhl et al, 1989), ethanol (Burrows et al, 1995;Granato and Van Pelt, 2003;Smith and Davies, 1990), cocaine (Harvey et al, 2001;Stanwood et al, 2001) and methyl mercury (Choi et al, 1981;Stoltenburg-Didinger and Markwort, 1990). While it would be desirable to increase the data set to better understand the relationship between chemical effects on neurite outgrowth in vitro and in vivo, a one-to-one correspondence may not be necessary in the context of chemical screening.…”

Section: Discussionmentioning

confidence: 99%

Developmental neurotoxicity testing in vitro: Models for assessing chemical effects on neurite outgrowth

2008

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Effects of early ethanol exposure on dendrite growth of cortical pyramidal neurons: inferences from a computational model

Cited by 33 publications

References 20 publications

Prenatal stress causes dendritic atrophy of pyramidal neurons in hippocampal CA3 region by glutamate in offspring rats

Prenatal stress causes dendritic atrophy of pyramidal neurons in hippocampal CA3 region by glutamate in offspring rats

Developmental Consequences of Fetal Exposure to Drugs: What We Know and What We Still Must Learn

Developmental neurotoxicity testing in vitro: Models for assessing chemical effects on neurite outgrowth

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