Abstract
Cognitive dysfunction in mice lacking proper glucocorticoid receptor dimerization
Highlights
Stress is commonly defined as a state of real or perceived threat to homeostasis [1]
In this study we analysed the behavioural phenotype of female FVB/NJ mice harbouring a point mutation in the glucocorticoid receptor (GR), known as GRdim/dim, under baseline and under chronically elevated corticosterone levels
We analysed expression levels of selected genes that have been shown to be differentially regulated by (i) corticosterone [72,73,74] and stress [75], (ii) in major depressive disorders in the hippocampus [29], and (iii) play an important role in cognitive processes especially in learning impairments reported in preclinical models and clinical population of depression [76,77,78,79,80]
Summary
Stress is commonly defined as a state of real or perceived threat to homeostasis [1]. Short-term stress serves as an important mechanism to survive, while chronic stress is detrimental and an important contributor to major psychiatric disorders such as depression and anxiety [2]. Glucocorticoids and memory loss collectively known as the stress response [3, 4]. Chronic elevation of the stress response will affect neuronal functioning by inhibiting neurogenesis, proper synaptic pruning and changes in neurotransmitter systems [5, 6], and induce a wide range of behavioral changes including cognitive processes. One of the hormones released in response to stress, are glucocorticoids (GCs). The physiological functions of GCs include regulation of metabolic homeostasis, immune function, cell proliferation and survival, and behaviour including cognition [7,8,9], while endogenous excess or dysregulation of GCs is associated with mood changes, including depression and hypomanic symptomatology [10]
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