Stressful events are known to increase the risk of depression but predisposing factors are not clearly understood. This study describes the efforts of Blugeot and colleagues to characterize vulnerability traits for the development of depressive disorders in adult animals. Four weeks after a priming stressful event, serum corticosterone concentrations were observed to return to control values in all animals, but other biological parameters returned to basal level in only 58% of animals (labeled “nonvulnerable” animals). In contrast, 42% of animals displayed persistent decreases in serum and hippocampal brain-derived neurotrophic factor (BDNF) concentrations, reduced hippocampal volume, reduced neurogenesis, CA3 dendritic retraction and reduced spine density, as well as amygdala neuron hypertrophy. This “vulnerable” group also showed a rise in serum corticosterone and a “depressive” phenotype after mild stress, in contrast to “nonvulnerable” animals. Intracerebroventricular administration of a selective TrkB receptor agonist, dampened the development of the “depressive” phenotype. The authors discuss the concept that these changes represent latent vulnerability traits underlying the emergence of depression and they identify the presence of low BDNF with normal corticosterone serum concentrations as a predictive vulnerability marker for depression.
Blugeot A et al., Vulnerability to Depression: From Brain Neuroplasticity to Identification of Biomarkers.
J. Neuroscience 31(36): 12889-12899 (2011).
http://www.jneurosci.org/content/31/36/12889.abstract?etoc