Effects of prenatal ethanol exposure on dendritic spines of layer V pyramidal neurons in the somatosensory cortex of the rat

Galofré, E; Ferrer, Isidró; Fabregues, I.; López-Tejero, Dolores

doi:10.1016/0022-510x(87)90095-5

Cited by 31 publications

(14 citation statements)

References 29 publications

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“…This postmortem study involved a 4-month-old microcephalic child whose mother suffered from alcohol addiction and drank throughout pregnancy, and compared to age-matched controls. Similar findings have been reported in rat somatosensory cortex after exposure throughout rat gestation, although the effect was transient and resolved by adulthood (Galofre et al, 1987). EtOH exposure from E5 (embryonic day 5) to P0 (postnatal day 0, parturition) via dam intubation also showed that dendritic spine development on pyramidal neurons in visual cortex was delayed through adolescence in mice, with higher amounts of EtOH showing a more severe delay (Cui et al, 2010).…”

Section: Microglial Roles In Fasdsupporting

confidence: 87%

What the Spectrum of Microglial Functions Can Teach us About Fetal Alcohol Spectrum Disorder

Wong

Stowell

Majewska

2017

Front. Synaptic Neurosci.

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Alcohol exposure during gestation can lead to severe defects in brain development and lifelong physical, behavioral and learning deficits that are classified under the umbrella term fetal alcohol spectrum disorder (FASD). Sadly, FASD is diagnosed at an alarmingly high rate, affecting 2%-5% of live births in the United States, making it the most common non-heritable cause of mental disability. Currently, no standard therapies exist that are effective at battling FASD symptoms, highlighting a pressing need to better understand the underlying mechanisms by which alcohol affects the developing brain. While it is clear that sensory and cognitive deficits are driven by inappropriate development and remodeling of the neural circuits that mediate these processes, alcohol's actions acutely and long-term on the brain milieu are diverse and complex. Microglia, the brain's immune cells, have been thought to be a target for alcohol during development because of their exquisite ability to rapidly detect and respond to perturbations affecting the brain. Additionally, our view of these immune cells is rapidly changing, and recent studies have revealed a myriad of microglial physiological functions critical for normal brain development and long-term function. A clear and complete understanding of how microglial roles on this end of the spectrum may be altered in FASD is currently lacking. Such information could provide important insights toward novel therapeutic targets for FASD treatment. Here we review the literature that links microglia to neural circuit remodeling and provide a discussion of the current understanding of how developmental alcohol exposure affects microglial behavior in the context of developing brain circuits.

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Section: Microglial Roles In Fasdsupporting

confidence: 87%

What the Spectrum of Microglial Functions Can Teach us About Fetal Alcohol Spectrum Disorder

Wong

Stowell

Majewska

2017

Front. Synaptic Neurosci.

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“…9A) and calibrated the model such that the maximum conductance for a single spine was kept constant ( input ϭ 3 ms, g max ϭ 0.28 nS) and produced a subthreshold EPSPs at the soma. The distal spine was located at a constant distance from the soma, whereas the location of the proximal spine varied such that the two spines had an interspine distance that varied from 5 to 5.24 m. This interspine distance corresponds with an approximate spine density of 2.5 spines/5 m dendritic branch, which is within the lower range of spine densities observed in vivo in the hippocampus (Garcia-Lopez et al 2006). Within predefined parameters (see METHODS), when either the two thin (Fig.…”

Section: Spine Shape Limits Effective Interspine Distancementioning

confidence: 88%

“…The compartments closest and farthest from the soma contained no spines. This follows previous quantitative morphological studies on dorsal horn neurons that show no or few spines close to the soma, increased spine density in medial portions of the branch, and decreased spine density at distal regions (Garcia-Lopez et al 2006;Ruiz-Marcos and Valverde 1969;Valverde and Ruiz-Marcos 1969). The spine density/distribution on the dendritic branch of the simplified neuron in the intact model used a total of six spines distributed at equally spaced intervals across a 350-m length of the dendrite.…”

Section: Simplified Neuron Morphologymentioning

confidence: 98%

“…Dimensional information about dendritic spines located on dorsal horn neurons is available from our previous report (Tan et al 2008) and we used spine geometries that fell within these published ranges to derive parameters for the spine neck, spine head, and spine volume (Calabrese et al 2006;Galofre et al 1987;Garcia-Lopez et al 2006;Harris and Kater 1994;Kim et al 2006). To construct spines and examine the effects of spine shape on the signal transduction onto the parent dendritic branch, we used a two-compartment model: spine neck and head.…”

Section: Modeling Dendritic Spinesmentioning

confidence: 99%

“…1D). To test the effects of these dendritic spine density/distribution changes, we modeled a simple neuron with spines distributed across a dendrite following a general distribution for spiny dorsal horn neurons in the spinal cord and cortical neurons (Garcia-Lopez et al 2006;RuizMarcos and Valverde 1969;Tan et al 2008;Valverde and Ruiz-Marcos 1969) (see METHODS). This model is shown in Fig.…”

Section: Increasing the Number Of Spines And Altering Spatial Distribmentioning

confidence: 99%

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Dendritic Spine Remodeling After Spinal Cord Injury Alters Neuronal Signal Processing

Tan

Choi

Waxman

et al. 2009

Journal of Neurophysiology

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Tan AM, Choi J-S, Waxman SG, Hains BC. Dendritic spine remodeling after spinal cord injury alters neuronal signal processing. J Neurophysiol 102: 2396 -2409, 2009. First published August 19, 2009 doi:10.1152/jn.00095.2009. Central sensitization, a prolonged hyperexcitability of dorsal horn nociceptive neurons, is a major contributor to abnormal pain processing after spinal cord injury (SCI). Dendritic spines are micron-sized dendrite protrusions that can regulate the efficacy of synaptic transmission. Here we used a computational approach to study whether changes in dendritic spine shape, density, and distribution can individually, or in combination, adversely modify the input-output function of a postsynaptic neuron to create a hyperexcitable neuronal state. The results demonstrate that a conversion from thin-shaped to more mature, mushroom-shaped spine structures results in enhanced synaptic transmission and fidelity, improved frequency-following ability, and reduced inhibitory gating effectiveness. Increasing the density and redistributing spines toward the soma results in a greater probability of action potential activation. Our results demonstrate that changes in dendritic spine morphology, documented in previous studies on spinal cord injury, contribute to the generation of pain following SCI.

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Overview on the structure, composition, function, development, and plasticity of hippocampal dendritic spines

2000

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There has been an explosion of new information on the neurobiology of dendritic spines in synaptic signaling, integration, and plasticity. Novel imaging and analytical techniques have provided important new insights into dendritic spine structure and function. Results are accumulating across many disciplines, and a step toward consolidating some of this work has resulted in Dendritic Spines of the Hippocampus. Leaders in the field provide a discussion at the level of advanced undergraduates, with sufficient detail to be a contemporary resource for research scientists. Critical reviews are presented on topics ranging from spine structure, formation, and maintenance, to molecular composition, plasticity, and the role of spines in learning and memory. Dendritic Spines of the Hippocampus provides a timely discussion of our current understanding of form and function at these excitatory synapses. We asked authors to include areas of controversy in their papers so as to distinguish results that are generally agreed upon from those where multiple interpretations are possible. We thank the contributors for their insights and thoughtful discussions. In this paper we provide background on the structure, composition, function, development, plasticity, and pathology of hippocampal dendritic spines. In addition, we highlight where each of these subjects will be elaborated upon in subsequent papers of this special issue of Hippocampus. Hippocampus 2000;10:501–511. © 2000 Wiley‐Liss, Inc.

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Effects of prenatal ethanol exposure on dendritic spines of layer V pyramidal neurons in the somatosensory cortex of the rat

Cited by 31 publications

References 29 publications

What the Spectrum of Microglial Functions Can Teach us About Fetal Alcohol Spectrum Disorder

What the Spectrum of Microglial Functions Can Teach us About Fetal Alcohol Spectrum Disorder

Dendritic Spine Remodeling After Spinal Cord Injury Alters Neuronal Signal Processing

Overview on the structure, composition, function, development, and plasticity of hippocampal dendritic spines

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