Abstract

Many studies have shown that chronic stress or corticosterone over-exposure in rodents leads to extensive dendritic remodeling, particularly of principal neurons in the CA3 hippocampal area and the basolateral amygdala. We here investigated to what extent genetic predisposition of mice to high versus low stress reactivity, achieved through selective breeding of CD-1 mice, is also associated with structural plasticity in Golgi-stained neurons. Earlier, it was shown that the highly stress reactive (HR) compared to the intermediate (IR) and low (LR) stress reactive mice line presents a phenotype, with respect to neuroendocrine parameters, sleep architecture, emotional behavior and cognition, that recapitulates some of the features observed in patients suffering from major depression. In late adolescent males of the HR, IR, and LR mouse lines, we observed no significant differences in total dendritic length, number of branch points and branch tips, summated tip order, number of primary dendrites or dendritic complexity of either CA3 pyramidal neurons (apical as well as basal dendrites) or principal neurons in the basolateral amygdala. Apical dendrites of CA1 pyramidal neurons were also unaffected by the differences in stress reactivity of the animals; marginally higher length and complexity of the basal dendrites were found in LR compared to IR but not HR mice. In the same CA1 pyramidal neurons, spine density of distal apical tertiary dendrites was significantly higher in LR compared to IR or HR animals. We tentatively conclude that the dendritic complexity of principal hippocampal and amygdala neurons is remarkably stable in the light of a genetic predisposition to high versus low stress reactivity, while spine density seems more plastic. The latter possibly contributes to the behavioral phenotype of LR versus HR animals.

Highlights

  • Altered reactivity and feedback regulation of the hypothalamopituitary-adrenal (HPA) axis in response to stressors are considered to be risk factors for the precipitation of psychiatric disorders, including major depression [1,2]

  • Chronic stress in adulthood or long-term over-exposure of rodents to corticosterone is associated with reduced dendritic complexity of CA3 pyramidal neurons [32,33,34,35]

  • A remarkable growth of principal neurons in the basolateral amygdala has been observed after chronic restraint stress [36,38]

Read more

Summary

Introduction

Altered reactivity and feedback regulation of the hypothalamopituitary-adrenal (HPA) axis in response to stressors are considered to be risk factors for the precipitation of psychiatric disorders, including major depression [1,2]. Elevated corticosteroid levels, during the circadian trough [7,8,9], as well as impaired responsiveness of the HPA axis to negative feedback by glucocorticoids have been reported in the majority of depressives [10,11]. To study the putative neuronal mechanism underlying changes in brain structure and function associated with altered HPA axis reactivity, several animal models are available. One of these models involves mouse lines selectively bred for differences in their corticosterone response to a moderate psychological stressor [27], eventually resulting in a distinct phenotype characterized by high (HR), intermediate (IR) or low (LR) reactivity of the HPA axis to acute stressors. HR mice show changes in sleep architecture, hyperactive coping behavior and cognitive deficits in several behavioral paradigms, i.e. a phenotype that recapitulates some features observed in depressive illness [28,29,30,31]

Methods
Results
Conclusion
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call