Chronic stress does not further exacerbate the abnormal psychoneuroendocrine phenotype of Cbg-deficient male mice.

Gabriela F. de Medeiros, Amandine M. Minni, Jean-Christophe Helbling, Marie-Pierre Moisan
Psychoneuroendocrinology. 2016-08-01; 70: 33-37
DOI: 10.1016/j.psyneuen.2016.04.014

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Chronic stress leads to a dysregulation of the hypothalamic-pituitary-adrenal
(HPA) axis which can constitute a base for pathophysiological consequences. Using
mice totally deficient in Corticosteroid binding globulin (CBG), we have
previously demonstrated the important role of CBG in eliciting an adequate
response to an acute stressor. Here, we have studied its role in chronic stress
situations. We have submitted Cbg ko and wild-type (WT) male mice to two
different chronic stress paradigms – the unpredictable chronic mild stress and
the social defeat. Then, their impact on neuroendocrine function – through
corticosterone and CBG measurement – and behavioral responses – via anxiety and
despair-like behavioral tests – was evaluated. Both chronic stress paradigms
increased the display of despair-like behavior in WT mice, while that from Cbg ko
mice – which was already high – was not aggravated. We have also found that
control and defeated (stressed) Cbg ko mice show no difference in the social
interaction test, while defeated WT mice reduce their interaction time when
compared to unstressed WT mice. Interestingly, the same pattern was observed for
corticosterone levels, where both chronic stress paradigms lowered the
corticosterone levels of WT mice, while those from Cbg ko mice remained low and
unaltered. Plasma CBG binding capacity remained unaltered in WT mice regardless
of the stress paradigm. Through the use of the Cbg ko mice, which only differs
genetically from WT mice by the absence of CBG, we demonstrated that CBG is
crucial in modulating the effects of stress on plasma corticosterone levels and
consequently on behavior. In conclusion, individuals with CBG deficiency, whether
genetically or environmentally-induced, are vulnerable to acute stress but do not
have their abnormal psychoneuroendocrine phenotype further affected by chronic


Auteurs Bordeaux Neurocampus