Related Experiment Video
Updated: Apr 17, 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
Behavioral training reverses global cortical network dysfunction induced by perinatal antidepressant exposure.
Xiaoming Zhou1, Jordan Y-F Lu2, Ryan D Darling2
1Key Laboratory of Brain Functional Genomics of Ministry of Education, Shanghai Key Laboratory of Brain Functional Genomics, School of Life Sciences, East China Normal University, Shanghai 200062, China; NYU-ECNU Institute of Brain and Cognitive Science, NYU Shanghai, Shanghai 200062, China; xmzhou@bio.ecnu.edu.cn michael.merzenich@positscience.com.
Early antidepressant exposure in rats caused auditory processing deficits, but behavioral training reversed these issues, including neural and neuromodulatory system impairments, suggesting therapeutic potential for autism.
Area of Science:
- Neuroscience
- Developmental Neuroscience
- Autism Research
Background:
- Autism is linked to abnormal cortical circuitry and impaired neurological processes controlling plasticity.
- Early life environmental factors, such as antidepressant exposure, may contribute to developmental neurological distortions.
Purpose of the Study:
- To investigate the potential for neuroplasticity-driven renormalization in a rodent model of autism induced by early-life antidepressant exposure.
- To evaluate the efficacy of behavioral training in reversing auditory processing deficits and associated neural impairments.
Main Methods:
- Developmental neurological distortions were induced in young rodents via subcutaneous injection of the antidepressant citalopram (postnatal days 1-10).
- Altered young rodents underwent intensive behavioral training using a modified go/no-go repetition-rate discrimination task.
- Auditory system processing, neuronal function, inhibitory GABAergic neurons, and neuromodulatory systems were assessed.
Main Results:
- Citalopram exposure impaired neuronal repetition-rate following capacity in the primary auditory cortex (A1).
- Behavioral training almost completely reversed targeted temporal processing deficits in the A1.
- Training also renormalized degraded parvalbumin inhibitory GABAergic neurons and their functions.
- Antidepressant-induced degradation of serotonergic and dopaminergic systems was sharply reversed by training.
Conclusions:
- Behavioral interventions can promote neuroplasticity and reverse developmental neurological distortions caused by early-life antidepressant exposure.
- These findings suggest promising avenues for neuroplasticity-based therapeutic strategies for individuals with autism spectrum disorder.
