Atomoxetine prevents working memory loss in hyperactive rats, mediating plastic changes in prefrontal cortex
Néstor I Martínez-Torres1, David González-Tapia2, Nallely Vázquez-Hernández3
1División de Neurociencias, Centro de Investigación Biomédica de Occidente, IMSS, Guadalajara, Jal., Mexico; Centro Universitario del Norte, Universidad de Guadalajara, Colotlán, Jal., Mexico.
Pharmacology, Biochemistry, and Behavior
|September 30, 2018
Summary
Attention Deficit Hyperactivity Disorder (ADHD) impairs visuospatial working memory. Atomoxetine (ATX) treatment reversed this cognitive loss by altering dendritic spine density in the prefrontal cortex.
Area of Science:
- Neuroscience
- Cognitive Science
- Pharmacology
Background:
- Attention Deficit Hyperactivity Disorder (ADHD) is linked to prefrontal cortex dysfunction and impaired visuospatial working memory (VWM).
- The synaptic mechanisms underlying ADHD-related cognitive deficits and the preventive effects of Atomoxetine (ATX) remain unclear.
Purpose of the Study:
- To investigate the synaptic plasticity involved in ADHD-related cognitive loss.
- To explore the mechanisms of Atomoxetine's preventive action on cognitive function in ADHD models.
Main Methods:
- Utilized neonatal 6-hydroxydopamine (6-OHDA) rat model of ADHD to assess allocentric VWM.
- Analyzed dendritic spine number and density on prefrontal cortex pyramidal neurons.
- Evaluated the effects of acute ATX treatment at 28 days of age.
Main Results:
- 6-OHDA lesions increased motor activity and reduced VWM, correlating with decreased thin dendritic spine density.
- ATX administration reversed cognitive deficits, decreasing thin spines and increasing mushroom spines.
- Hypothesized that increased memory-related mushroom spines contribute to cognitive restoration.
Conclusions:
- ADHD-related cognitive impairment may stem from a reduced proportion of learning-associated spines.
- Atomoxetine's therapeutic effect involves a shift in dendritic spine populations, favoring memory-related mushroom spines.
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