Selective effects of perinatal ethanol exposure in medial prefrontal cortex and nucleus accumbens.
- Authors
- Lawrence, R Charles; Otero, Nicha K H; Kelly, Sandra J
- Year
- 2012
- Journal
- Neurotoxicology and teratology
- PMID
- 21871563
- DOI
- 10.1016/j.ntt.2011.08.002
- PMCID
- PMC3245770
Ethanol exposure during development is the leading known cause of mental retardation and can result in characteristic physiological and cognitive deficits, often termed Fetal Alcohol Spectrum Disorders (FASD). Previous behavioral findings using rat models of FASD have suggested that there are changes in the nucleus accumbens (NAC) and medial prefrontal cortex (mPFC) following ethanol exposure during development. This study used a rat model of FASD to evaluate dendritic morphology in both the NAC and mPFC and cell number in the NAC. Dendritic morphology in mPFC and NAC was assessed using a modified Golgi stain and analyzed via three dimensional reconstructions with Neurolucida (MBF Bioscience). Cell counts in the NAC (shell and core) were determined using an unbiased stereology procedure (Stereo Investigator (MBF Bioscience)). Perinatal ethanol exposure did not affect neuronal or glial cell population numbers in the NAC. Ethanol exposure produced a sexually dimorphic effect on dendritic branching at one point along the NAC dendrites but was without effect on all other measures of dendritic morphology in the NAC. In contrast, spine density was reduced and distribution was significantly altered in layer II/III neurons of the mPFC following ethanol exposure. Ethanol exposure during development was also associated with an increase in soma size in the mPFC. These findings suggest that previously observed sexually dimorphic changes in activation of the NAC in a rat model of FASD may be due to altered input from the mPFC.
A) Representative neuron from a Golgi stained section of the rat mPFC corresponding to plates 8–12 of rat atlas (Paxinos and Watson 2006). This image is from a light microscope at 20X. B) This image is a reconstructed tracing resized to match the light microscope image. C) Details of the Golgi image and reconstructed image of a portion of the dendrite as defined by the rectangles in A and B.
LLM interpretation
This figure consists of light microscopy images and a digital reconstruction of a single neuron from the rat mPFC. Panel A shows a representative Golgi-stained neuron at 20X magnification, while Panel B provides a corresponding reconstructed tracing of the same cell. Panel C displays magnified views of a specific dendritic segment, comparing the original Golgi image to the reconstructed tracing.
Dendritic Branching in the Nucleus Accumbens (NAC). Perinatal ethanol exposure did not alter dendritic morphology in the NAC when sexes were combined. Data are collapsed across sex. Error bars represent SEMs and subject numbers are 12, 13, and 8 for the NC, IC and ET groups respectively. Inset: There was a significant increase in intersections in the ET females at 150 μm compared to NC males and IC females (p<0.05). ET males and NC females did not have any intersections in the 150 μm Sholl ring. Error bars represent SEMs and subject numbers are 7, 6 and 4 in NC, IC, and ET males respectively and 5, 7, and 4 for NC, IC and ET females respectively. The symbol * indicates significant differences from all other groups (p’s<0.05).
LLM interpretation
This figure consists of a main bar chart and an inset bar chart analyzing dendritic branching in the Nucleus Accumbens across three groups: NC, IC, and ET. The main chart shows the number of dendritic branches across four Sholl rings (50, 100, 150, and 200 $\mu$m), with a general trend of decreasing branch numbers as the ring distance increases. The inset focuses on the 150 $\mu$m Sholl ring, showing a significant increase in dendritic branches for ET females compared to all other sex-specific groups ($p < 0.05$), as indicated by an asterisk.
Soma Size (A) and Spine Density (B) in the Nucleus Accumbens. No significant differences in soma size or spine density were found across treatment groups. Data are collapsed across sex and error bars represent SEMs. Subject numbers are 12, 13, and 8 for the NC, IC and ET groups respectively.
LLM interpretation
This figure consists of two bar charts comparing measurements in the Nucleus Accumbens across three treatment groups: NC, IC, and ET. Panel A shows soma size ($\mu\text{m}^2$) and Panel B shows spine density ($\#/ \mu\text{m}$), with error bars representing SEMs. No statistically significant differences are indicated between the groups for either metric.
Dendritic Branching (A) and Soma Size (B) in mPFC. Intersections within the 150 μm Sholl rings were significantly decreased in the ET group relative to the IC group (p<0.05). Perinatal ethanol exposure induced an increase in soma size relative to the NC group only (p’s<0.05). Data are collapsed across sex and error bars represent SEMs. Subject numbers are are 12, 13, and 9 for the NC, IC and ET groups respectively. The symbol ** indicates significantly different from the IC group only and the symbol ++ indicates a significant difference from the NC group only (p’s < 0.05).
LLM interpretation
This figure consists of two bar charts comparing NC, IC, and ET groups in the mPFC. Panel A shows the number of dendritic branches across Sholl rings (50–300 $\mu$m), with a significant decrease in the ET group compared to the IC group at the 150 $\mu$m ring (**p < 0.05). Panel B shows soma size ($\mu\text{m}^2$), where the ET group is significantly larger than the NC group (++p < 0.05).
Spine Density in mPFC following perinatal ethanol exposure. Ethanol treatment resulted in a reduction in dendritic spine density compared to both control groups whether the data were separated by apical or basilar dendrites or combined across apical or basilar dendrites. Data are collapsed across sex and error bars represent SEMs. Subject numbers for this measure are 12, 13, and 9 for the NC, IC and ET groups respectively. The symbol * indicates significant differences from both control groups (p<0.05).
LLM interpretation
This bar chart compares dendritic spine density (#/µm) across three groups—NC (white), IC (grey), and ET (black)—within the mPFC. The data is categorized by area of the dendritic tree: combined basilar and apical dendrites, basilar dendrite, and apical dendrite. In all three categories, the ET group shows a lower spine density compared to the NC and IC groups, with asterisks (*) indicating a statistically significant difference (p<0.05) from both control groups.
Spine distribution in the mPFC as determined by spine density per Sholl ring (A) was significantly reduced at 50μm and 100 μm compared to both control groups. Spines were reduced in the ET group compared to the IC group only at 150 μm. Data are collapsed across sex and error bars represent SEMs. Subject numbers for this measure are NC (12), IC (13), ET (9). * indicates a significant difference from both control groups and the symbol ** indicates a significant difference from the IC group only (p<0.05).
LLM interpretation
This bar chart displays spine density (number per $\mu$m) across six Sholl rings (50–300 $\mu$m from the soma) for three groups: NC, IC, and ET. The ET group shows a reduction in spine density compared to both control groups at 50 $\mu$m and 100 $\mu$m (marked by *), and a reduction compared only to the IC group at 150 $\mu$m (marked by **). Error bars represent SEMs, and the differences at these three distances are statistically significant ($p < 0.05$).
Spine distribution in the mPFC at the 50 μm Sholl ring. At 50 μm, females across all groups had increased spine density relative to males. Error bars represent SEMs and subject numbers are 7, 6, and 4 in NC, IC and ET males respectively and 5, 7, and 5 in NC, IC and ET females respectively.
LLM interpretation
This bar chart displays spine density (#/μm) in the mPFC at the 50 μm Sholl ring across three treatment groups: NC, IC, and ET. In all three groups, females (indicated by the ♀ symbol) exhibit higher mean spine density compared to males (indicated by the ♂ symbol). The y-axis measures spine density, and error bars represent the standard error of the mean (SEM).
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| Impact of Prenatal Alcohol Exposure on Cerebral Cortex Development. | Oskera L et al. | — | 2026 | → |
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| Deliberative Behaviors and Prefrontal-Hippocampal Coupling are Disrupted in a Rat Model of Fetal Alcohol Spectrum Disorders | Rosenblum HL et al. | — | 2024 | — |
| Gestational ethanol exposure impairs motor skills in female mice through dysregulated striatal dopamine and acetylcholine function. | Bariselli S et al. | — | 2023 | → |
| Moderate prenatal alcohol exposure produces sex-specific social impairments and attenuates prelimbic excitability and amygdala-cortex modulation of adult social behaviour. | Przybysz KR et al. | — | 2023 | → |
| Fluoxetine exposure throughout neurodevelopment differentially influences basilar dendritic morphology in the motor and prefrontal cortices. | Maloney SE et al. | — | 2022 | → |
| Representation of prefrontal axonal efferents in the thalamic nucleus reuniens in a rodent model of fetal alcohol exposure during third trimester. | Smith EA et al. | — | 2022 | → |
| Corticostriatal Circuit Models of Cognitive Impairments Induced by Fetal Exposure to Alcohol. | Bariselli S et al. | — | 2021 | → |
| Dynamics of microglia and dendritic spines in early adolescent cortex after developmental alcohol exposure. | Wong EL et al. | — | 2021 | → |
| Executive functioning-specific behavioral impairments in a rat model of human third trimester binge drinking implicate prefrontal-thalamo-hippocampal circuitry in Fetal Alcohol Spectrum Disorders. | Gursky ZH et al. | — | 2021 | → |
| Maternal Ethanol Exposure Acutely Elevates Src Family Kinase Activity in the Fetal Cortex. | Wang D et al. | — | 2021 | → |
| Neurodevelopmental signatures of narcotic and neuropsychiatric risk factors in 3D human-derived forebrain organoids. | Notaras M et al. | — | 2021 | → |
| Increased ethanol intake is associated with social anxiety in offspring exposed to ethanol on gestational day 12. | Diaz MR et al. | — | 2020 | → |
| Preclinical methodological approaches investigating of the effects of alcohol on perinatal and adolescent neurodevelopment. | Bailey CDC et al. | — | 2020 | → |
| Cholinergic rescue of neurocognitive insult following third-trimester equivalent alcohol exposure in rats. | Heroux NA et al. | — | 2019 | → |
| Effects of neonatal ethanol on cerebral cortex development through adolescence. | Smiley JF et al. | — | 2019 | → |
| Neonatal ethanol exposure impairs long-term context memory formation and prefrontal immediate early gene expression in adolescent rats. | Heroux NA et al. | — | 2019 | → |
| Nucleus reuniens of the midline thalamus of a rat is specifically damaged after early postnatal alcohol exposure. | Gursky ZH et al. | — | 2019 | → |
| Striatal morphological and functional alterations induced by prenatal alcohol exposure. | Ma YY | — | 2019 | → |
| Impairment of the context preexposure facilitation effect in juvenile rats by neonatal alcohol exposure is associated with decreased Egr-1 mRNA expression in the prefrontal cortex. | Jablonski SA et al. | — | 2018 | → |
| Meta-Analyses of Externalizing Disorders: Genetics or Prenatal Alcohol Exposure? | Wetherill L et al. | — | 2018 | → |
| Prenatal alcohol exposure disrupts male adolescent social behavior and oxytocin receptor binding in rodents. | Holman PJ et al. | — | 2018 | → |
| DNA Methylation program in normal and alcohol-induced thinning cortex. | Öztürk NC et al. | — | 2017 | → |
| Effects of prenatal binge-like ethanol exposure and maternal stress on postnatal morphological development of hippocampal neurons in rats. | Jakubowska-Dogru E et al. | — | 2017 | → |
| Neurotrophins in the Brain: Interaction With Alcohol Exposure During Development. | Boschen KE et al. | — | 2017 | → |
| Risk-taking, locomotor activity and dopamine levels in the nucleus accumbens and medial prefrontal cortex in male rats treated prenatally with alcohol. | Muñoz-Villegas P et al. | — | 2017 | → |
| Behavioral deficits induced by third-trimester equivalent alcohol exposure in male C57BL/6J mice are not associated with reduced adult hippocampal neurogenesis but are still rescued with voluntary exercise. | Hamilton GF et al. | — | 2016 | → |
| Effects of ethanol exposure and withdrawal on dendritic morphology and spine density in the nucleus accumbens core and shell. | Peterson VL et al. | — | 2015 | → |
| Mechanisms of Action and Persistent Neuroplasticity by Drugs of Abuse. | Korpi ER et al. | — | 2015 | → |
| Moderate prenatal alcohol exposure enhances GluN2B containing NMDA receptor binding and ifenprodil sensitivity in rat agranular insular cortex. | Bird CW et al. | — | 2015 | → |
| Selective reduction of cerebral cortex GABA neurons in a late gestation model of fetal alcohol spectrum disorder. | Smiley JF et al. | — | 2015 | → |
| Voluntary exercise partially reverses neonatal alcohol-induced deficits in mPFC layer II/III dendritic morphology of male adolescent rats. | Hamilton GF et al. | — | 2015 | → |
| Activity and social behavior in a complex environment in rats neonatally exposed to alcohol. | Boschen KE et al. | — | 2014 | → |
| Brain development, experience, and behavior. | Kolb B et al. | — | 2014 | → |
| Postnatal ethanol exposure simplifies the dendritic morphology of medium spiny neurons independently of adenylyl cyclase 1 and 8 activity in mice. | Susick LL et al. | — | 2014 | → |
| Differential striatal spine pathology in Parkinson's disease and cocaine addiction: a key role of dopamine? | Villalba RM et al. | — | 2013 | → |
| Long-lasting neural circuit dysfunction following developmental ethanol exposure. | Sadrian B et al. | — | 2013 | → |
| Stress-induced grey matter loss determined by MRI is primarily due to loss of dendrites and their synapses. | Kassem MS et al. | — | 2013 | → |
| The atypical dopamine transport inhibitor, JHW 007, prevents amphetamine-induced sensitization and synaptic reorganization within the nucleus accumbens. | Velázquez-Sánchez C et al. | — | 2013 | → |
| Ethanol-induced disruption of Golgi apparatus morphology, primary neurite number and cellular orientation in developing cortical neurons. | Powrozek TA et al. | — | 2012 | → |
| Experience and the developing prefrontal cortex. | Kolb B et al. | — | 2012 | → |
| Long-term consequences of developmental alcohol exposure on brain structure and function: therapeutic benefits of physical activity. | Klintsova AY et al. | — | 2012 | → |
| Prenatal ethanol exposure stimulates neurogenesis in hypothalamic and limbic peptide systems: possible mechanism for offspring ethanol overconsumption. | Chang GQ et al. | — | 2012 | → |