Abstract
Chronic stress has detrimental effects on physiology, learning and memory and is involved in the development of anxiety and depressive disorders. Besides changes in synaptic formation and neurogenesis, chronic stress also induces dendritic remodeling in the hippocampus, amygdala and the prefrontal cortex. Investigations of dendritic remodeling during development and treatment of stress are currently limited by the invasive nature of histological and stereological methods. Here we show that high field diffusion-weighted MRI combined with quantitative biophysical modeling of the hippocampal dendritic loss in 21 day restraint stressed rats highly correlates with former histological findings. Our study strongly indicates that diffusion-weighted MRI is sensitive to regional dendritic loss and thus a promising candidate for non-invasive studies of dendritic plasticity in chronic stress and stress-related disorders.
Highlights
The adverse effects of chronic stress on physiology, learning and memory are well described [1] and are known to be involved in the development of anxiety disorders such as post-traumatic stress disorder (PTSD) and major depressive illness [2]
In a 21 day restraint-stressed rat model we found significantly lower DWI measured neurite density in the hippocampal CA3 apical areas compared to controls
No differences were found in the stratum oriens region or the pyramidal cell layer
Summary
The adverse effects of chronic stress on physiology, learning and memory are well described [1] and are known to be involved in the development of anxiety disorders such as post-traumatic stress disorder (PTSD) and major depressive illness [2]. Being of central importance in spatial learning and memory, the hippocampus is a highly vulnerable brain structure susceptible to the damaging effects of chronic stress and circulating adrenal steroids [4]. There is profound evidence that chronic high level stress or glucocorticoid administration in rats and primates is associated with loss of apical dendritic material of pyramidal neurons and even neuronal death [8,9], especially in CA3 [9,10], and in the CA1 region [11]. In moderate durations of stress or glucocorticoid administration, this effect has been reported in CA3 pyramidal neurons and correlates with a reduced performance in both short-term spatial and other types of memory tasks in rats [12,13,14,15,16,17,18]
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