Intermittent Social Isolation during Early Adolescence Induces Prefrontal and Cingulate Neuro-Morphological Changes during Mid-Adolescence in the Wistar Kyoto Rat Model of Endogenous Depression
Reshma A Shetty, Monika SadanandaObjectives
A stressful situation plays an important role in the pathogenesis of mental illness. Symptoms of these conditions alter the structure and function of these brains. Adverse environmental changes in adolescence rats lead to a drastic shift in behaviour and neuronal morphology as it continues to mature. During pre-pubertal and pubertal periods, young rats spend much of the time in social play behaviour, which decreases with age. The post-weaning environmental experience of adolescent rats plays an important role in shaping their adult behaviour, neuronal morphology and neurochemistry. A common procedure used to manipulate the experiences of adolescent rats involves post-weaning isolation housing.
Material and Methods
Here, we examined mild 6 hrs of isolation stress altering dendritic morphology in the limbic areas, namely Prelimbic, Cingulate cortex area 1, Cingulate cortex area 2, in adolescent male Wistar Kyoto Rats, an inbred strain, which is a putative animal model of endogenous depression. On the last day of isolation, animals were perfused, and brains were stained using silver nitrate. Neurons of the limbic areas were drawn using a camera lucida and performed Sholl analyses. Data were analysed by student t test. p <0.05 was considered significant.
Results
In comparison to controls, 6 hours of social isolation stress during adolescence dramatically decreased dendritic length and branching in pyramidal neurons of the prelimbic, cingulate cortex area 1, and cingulate cortex area 2. These results suggest that limbic cortical areas undergo stress-induced dendritic remodelling.
Conclusion
Reduced dendritic complexity is one of the anatomical alterations in the limbic brain caused by brief social isolation during adolescence. These changes may increase susceptibility to stress-related diseases by impairing neural connections and contributing to deficiencies in cognitive and emotional functioning.