To begin to search for the molecular underpinnings of the opposing effects of male sex chromosome complement and circulating testosterone on anxiety-like behavior, we examined expression of several mood-related genes in the frontal cortex of FCG mice.
Despite the high prevalence of anxiety in the general population, few studies have focused on the relationship between inflammatory biomarkers and anxiety, and the relation of anxiety to circulating leptin and adiponectin levels has never been examined in a study large enough to allow adjustment for possible confounders.
Additionally, we saw a potent effect of circulating testosterone to decrease anxiety-like behavior in UCMS-exposed mice, consistent with prior evidence in the literature [ 98].
Since "intact" male mice exhibit lower emotionality than females [ 90] and since we observed a more robust effect of circulating testosterone on lowering anxiety-like behaviors compared to the anxiogenic effect of XY genetic sex, circulating testosterone seems to "win out" in a normal male; the end result being lower anxiety-like behavior in males [ 89].
Of note, our previous study in these same FCG mice found that circulating testosterone potently decreased anxiety-like behaviors [ 13]; thus, future studies will aim to identify genes and proteins whose expression is altered in anti-disease directions by circulating testosterone treatment.
The stress from the surgical pathology, pain and anxiety may increase circulating catecholamine levels in patients requiring an emergency laparotomy.
Specifically, XY mice, regardless of gonadal sex or adult circulating testosterone treatment, exhibited increased anxiety-like behavior relative to XX mice.
We demonstrate herein that higher phobic anxiety is associated with higher circulating leptin levels that remained significant after adjustment for possible confounders and other biomarkers.
While our analyses used biobehavioral factors as the predictors in the models, sleep disturbance may in turn exacerbate depression and anxiety and may even alter circulating IL-6.
To our knowledge, this is the first study to document increased circulating vascular adhesion markers in a chronic anxiety state independently of other confounding factors, and these data need to be confirmed by future studies.
Conclusions: Our findings do not lend support to a role for maternal anxiety or second trimester increases in circulating stress hormones in the pathogenesis of PE.
