Deep brain stimulation mediates neurotrophin signaling in an animal model of antidepressant resistance

Chronic adrenocorticotropic hormone administration at circadian nadir produces an antidepressant resistance animal model that does not present with an altered plasma corticosterone profile nor changes in hippocampal brain derived neurotrophic factor and its receptor. Acute and chronic infralimbic deep brain stimulation elicited an antidepressant response in this animal model, which appears to be associated with changes in gene and protein expression of key intracellular mediators of neurotrophic factor signaling. Together, these findings stand to make important positive impacts on treatment strategies for one of the most debilitating and prevalent disorders of the modern era and suggest that antidepressant treatment response may involve mechanisms distinct from chronic stress-mediated induction of depression-like behavioral phenotypes.

A magic pill? A qualitative analysis of patients' views on the role of antidepressant therapy in inflammatory bowel disease (IBD).

BACKGROUND: Studies with healthy volunteers have demonstrated that antidepressants can improve immunoregulatory activity and thus they may have a potential to positively impact the disease course in inflammatory bowel disease (IBD), a chronic and incurable condition. However, patients' views on the role of antidepressants in the management of their IBD are unknown. Thus, this study aimed to explore patients' experiences and opinions regarding the effect of antidepressants on IBD course before possibly undertaking future treatment trials with antidepressants. METHODS: Semi-structured in-depth interviews with open-ended questions were conducted with a randomly selected sample of IBD patients recruited at the Australian public hospital IBD clinic and currently receiving antidepressants. A qualitative content analysis was undertaken to summarise patients' responses. A Visual Analogue Scale was used to provide a quantitative assessment of patients' experiences with antidepressants. RESULTS: Overall, 15 IBD sufferers currently on antidepressants (nine females, six males) were interviewed. All 15 reported a positive response to antidepressants reporting they improved their quality of life, with minimal side-effects. Five patients (33.3%) felt the antidepressant had specifically improved their IBD course. Three patients noted how they believed the reduction in feelings of stress mediated the positive influence of the antidepressant on IBD course. Ten patients (66.7%) felt the antidepressants had not specifically influenced their IBD. Nine patients (60.0%) had a generally positive attitude towards antidepressants, four patients (26.7%) were ambivalent, and two patients (13.3%) held a negative view towards antidepressants. Twelve patients (80.0%) stated that they would be willing to participate in clinical trials. CONCLUSIONS: Antidepressants seem to be well tolerated by IBD patients. One third of patients reported an observable improvement of their IBD under the influence of this treatment. The positive attitude towards antidepressants in these participants may make the conduct of clinical trials to further assess for any specific role on IBD course feasible. However, due to a small sample size, a qualitative nature of this study and in light of the results of studies on other populations indicating reluctance to taking antidepressants at least in some patients, these results should be interpreted with caution until confirmed in quantitative studies.