Acute psychosocial stress increases serum BDNF levels: an antagonistic relation to cortisol but no group differences after mental training

Abstract

Brain-derived neurotrophic factor (BDNF) is an essential facilitator of neuronal plasticity. By counteracting the adverse effects of excessive stress-induced glucocorticoid signaling, BDNF has been implicated as a resilience factor to psychopathology caused by chronic stress. Insights into the effects of acute stress on peripheral BDNF levels in humans are inconclusive. The short-term interplay between BDNF and cortisol in response to acute psychosocial stress remains unexplored. Furthermore, it is unknown whether mental training that is effective at reducing cortisol reactivity can also influence BDNF during acute stress. In the current study, we investigated serum BDNF levels during an acute psychosocial stress paradigm, the Trier Social Stress Test (TSST), in 301 healthy participants (178 women, mean age = 40.65) recruited as part of the ReSource Project, a large-scale mental training study consisting of three distinct 3-month training modules. Using a cross-sectional study design, we first examined the relationship between BDNF and salivary cortisol in a control group with no mental training. Subsequent analyses focused on differences in BDNF stress levels between control and mental training groups. We show that serum BDNF is indeed stress-sensitive, characterized by a significant post-stress increase and subsequent decline to recovery. While respective increases in BDNF and cortisol were not associated, we found two indications for an antagonistic relationship. Higher BDNF peaks after stress were associated with steeper cortisol recovery. On the other hand, the magnitude of the cortisol stress response was linked to steeper BDNF recovery after stress. BDNF levels were not modulated by any of the mental training modules. Providing novel evidence for the dynamics of BDNF and cortisol during acute stress, our findings may further inform research on the physiological mechanisms involved in stress chronification and the associated health risks.

Acute increases in brain-derived neurotrophic factor in plasma following physical exercise relates to subsequent learning in older adults

“…It is conceivable that factors common to all interventions, such as the blood sampling procedure or the unfamiliar environment and test procedure, reflected exposure to non-physical stressors. Mechanistic links have indeed been made that BDNF and glucocorticoids work in conjunction in response to acute stress but little is known about the acute effects of non-physical stressors on peripheral BDNF concentrations in humans 43,44 . Considering previous demonstrations of decreasing or stable resting BDNF concentrations in plasma over the course of the day, we consider diurnal variation in plasma BDNF as a less likely account for the gradual and sizeable increases reported here 45,46 .…”

Clustering suicidal phenotypes and genetic associations with brain-derived neurotrophic factor in patients with substance use disorders

“…Finally, the lack of data regarding childhood trauma and impulsivity is a potentially important limitation of this study. Sexual abuse notably increases the risk for SA in populations with mental disorders 83 , especially for ‘recurrent’ SA 84 , possibly in interaction with variations in the BDNF gene 22 , 85 . However, the latter associations rather regarded depression and anxiety than SA itself 24 , 72 .…”

“…Brain-derived neurotrophic factor (BDNF), and associated inducers and neurotrophins (the ‘neurotrophic pathway’) is a promising candidate, being involved in the neurobiological processes of stress reactivity 22 , brain plasticity in response to chronic drug use 23 and suicidal behavior. Neurotrophins are growth factors involved in the regulation of cerebral plasticity, notably synaptic changes in structure, number and connectivity.…”

Circulating neurotrophins and hemostatic risk factors of atherothrombotic cardiovascular disease at baseline and during sympathetic challenge: the SABPA study

“…The VWF, mediating platelet adhesion and aggregation in ACS 21 , fibrinogen and D-dimer, indicating fibrin formation, although not PAI-1, have been shown to be acute stress-responsive hemostatic factors 22 . Circulating levels of BDNF and S100B were also found to be responsive to acute mental stress in humans 23 and to restraint stress in rats 24 , respectively. Studies on whether circulating levels of neurotrophins, both at baseline and during stress, are associated with stress-induced hypercoagulability could provide new insight into the pathophysiology of the brain–heart link in ACS.…”