Related Experiment Video
Updated: Aug 25, 2026
The Use of Trace Eyeblink Classical Conditioning to Assess Hippocampal Dysfunction in a Rat Model of Fetal Alcohol Spectrum Disorders
Published on: August 5, 2017
Perinatal choline supplementation does not mitigate motor coordination deficits associated with neonatal alcohol
Jennifer D Thomas1, Teresa M O'Neill, Hector D Dominguez
1Center for Behavioral Teratology, Department of Psychology, San Diego State University, 6363 Alvarado Ct. Ste 209, San Diego, CA 92120, USA. thomas3@mail.sdsu.edu
Insights
Perinatal choline supplementation did not improve motor deficits in rats exposed to alcohol during development. These findings suggest choline is more effective for cognitive, not motor, deficits from prenatal alcohol exposure.
Area of Science:
- Neuroscience
- Developmental Biology
- Pharmacology
Background:
- Prenatal alcohol exposure (PAE) disrupts brain development, causing behavioral issues like learning deficits, hyperactivity, and motor dysfunction.
- Perinatal choline supplementation has previously shown promise in ameliorating alcohol-induced learning and hyperactivity deficits.
Purpose of the Study:
- To investigate if perinatal choline supplementation can reduce motor deficits caused by PAE during the third trimester equivalent brain growth spurt.
- To determine the task specificity of choline's beneficial effects on behavioral development following PAE.
Main Methods:
- Male neonatal rats were exposed to alcohol (6.6 g/kg/day) from postnatal days 4-9 using artificial rearing.
- Subjects received either choline chloride or saline injections from postnatal days 4-30.
- Motor performance was assessed on a parallel bar task on postnatal days 35-37.
Main Results:
- Ethanol-exposed rats exhibited significant motor impairments compared to control groups.
- Perinatal choline treatment did not significantly alter motor performance in either ethanol-exposed or control rats.
- Choline's beneficial effects appear to be task-specific, primarily impacting cognitive rather than motor functions.
Conclusions:
- Perinatal choline supplementation does not mitigate motor deficits induced by developmental alcohol exposure.
- Choline supplementation may be more effective in addressing cognitive deficits associated with PAE than motor deficits.
Abstract:
Prenatal alcohol exposure can disrupt brain development, leading to a variety of behavioral alterations including learning deficits, hyperactivity, and motor dysfunction. We have been investigating the possibility that perinatal choline supplementation may effectively reduce the severity of alcohol's adverse effects on behavioral development. We previously reported that perinatal choline supplementation can ameliorate alcohol-induced learning deficits and hyperactivity in rats exposed to alcohol during development. The present study examined whether perinatal choline supplementation could also reduce the severity of motor deficits induced by alcohol exposure during the third trimester equivalent brain growth spurt. Male neonatal rats were assigned to one of three treatment groups. One group was exposed to alcohol (6.6 g/kg/day) from postnatal days (PD) 4 to 9 via an artificial rearing procedure. Artificially and normally reared control groups were included. One half of subjects from each treatment received daily subcutaneous injections of a choline chloride solution from PD 4 to 30, whereas the other half received saline vehicle injections. On PD 35-37, subjects were tested on a parallel bar motor task, which requires both balance and fine motor coordination. Ethanol-exposed subjects exhibited significant motor impairments compared to both control groups whose performance did not differ significantly from one another. Perinatal choline treatment did not affect motor performance in either ethanol or control subjects. These data indicate that the beneficial effects of perinatal choline supplementation in ethanol-treated subjects are task specific and suggest that choline is more effective in mitigating cognitive deficits compared to motor deficits associated with developmental alcohol exposure.
