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Updated: Feb 15, 2026

Ballistic Labeling of Pyramidal Neurons in Brain Slices and in Primary Cell Culture
Published on: April 2, 2020
Neonatal Ethanol and Choline Treatments Alter the Morphology of Developing Rat Hippocampal Pyramidal Neurons in
C M Goeke1, M L Roberts2, J G Hashimoto1
1VA Portland Health Care System, Portland, OR 97239, USA; Department of Behavioral Neuroscience, Oregon Health & Science University, Portland, OR 97239, USA.
Insights
Developmental ethanol (EtOH) exposure increased apical dendrite complexity in rat pups. Choline (Chol) treatment alone decreased dendritic length and arborization, and did not rescue EtOH-induced changes in hippocampal neurons.
Area of Science:
- Neuroscience
- Developmental Biology
- Toxicology
Background:
- Fetal Alcohol Spectrum Disorders (FASDs) cause neurobehavioral deficits.
- A rat model mimics FASDs using gestational ethanol (EtOH) exposure.
- Choline (Chol) has shown promise in ameliorating EtOH-induced behavioral changes.
Purpose of the Study:
- To investigate the effects of EtOH and Chol on hippocampal CA1 pyramidal neuron morphology.
- To analyze changes in dendritic complexity and parameters following neonatal exposure.
Main Methods:
- Golgi-Cox staining was used to visualize neurons in Sprague-Dawley rat pups.
- Neurolucida tracing and analysis quantified morphometric parameters of CA1 pyramidal neurons.
- Neonatal rats received daily intragastric intubation of EtOH and/or Chol.
Main Results:
- EtOH exposure increased apical dendrite complexity in both male and female pups.
- EtOH did not significantly alter basal dendrite parameters.
- Chol treatment alone decreased basal dendrite length and number in males; co-treatment did not reverse EtOH effects.
Conclusions:
- Developmental EtOH exposure may lead to premature neuronal maturation and restricted plasticity.
- Choline treatment appears to delay normal neuronal maturation, potentially prolonging the plasticity window.
- Chol did not prevent EtOH-induced morphological changes in hippocampal neurons in this study.
Abstract:
Some of the neurobehavioral deficits identified in children with Fetal Alcohol Spectrum Disorders (FASDs) have been recapitulated in a binge model of gestational third trimester-equivalent ethanol (EtOH) exposure, in which Sprague-Dawley rats are intragastrically intubated between post-natal day (PD) 4 and PD9 with high doses of EtOH. In this model, the ameliorating effects of choline (Chol) administration on hippocampus-dependent behaviors altered by EtOH have also been extensively documented. In the present study, we investigated the effects of EtOH (5 g/kg/day) and/or Chol (100 mg/kg/day) on morphometric parameters of CA1 pyramidal neurons by Golgi-Cox staining followed by Neurolucida tracing and analysis. We found that EtOH increased apical dendrite complexity in male and female pups neonatally exposed to EtOH. EtOH did not significantly affect basal dendrite parameters in female and male rats. Interestingly, Chol treatments decreased basal dendrites' length, number, and maximal terminal distance in male pups. When pups were co-treated with EtOH and Chol, Chol did not rescue the effect of EtOH. In conclusion, EtOH increases while Chol decreases dendritic length and arborization of hippocampal CA1 neurons in PD9 rats. We hypothesize that developmental EtOH exposure induces a premature maturation of neurons, leading to early restriction of neuronal plasticity while Chol treatments delay the normal program of neuronal maturation and therefore prolong the window of maximal plasticity. Chol does not prevent the effects of developmental alcohol exposure on hippocampal pyramidal neurons' morphology characterized in the present study, although whether prolonged Chol administration after developmental EtOH exposure rectifies EtOH damage remains to be assessed.
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