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The environment could have long lasting effects on the individual phenotype through developmental plasticity. Early environmental enrichment exerts profound biological effects, most of which are quite beneficial ones. To explore the enduring effects of rearing condition quality on BDNF(1) responses, we reared male Wistar rats from weaning to young-adulthood in three different environmental conditions: 1. Enriched 2. Standard, and 3. Isolated. Then, at the age of 16 weeks, 10 rats from each group were randomly chosen and allocated to six common mix cages. They were kept together for 14 weeks. At the end of the experiment, each rat received ten inescapable foot-shocks. Twelve hours later, the BDNF contents of the amygdala and CA1 sub-region of the dorsal hippocampus were measured. The serum BDNF levels, hematocrit values as well as brain and testis weights were also measured. Results showed that the environmental enrichment led to stronger dorsal hippocampal BDNF response and higher serum BDNF levels, while rats from standard laboratory condition showed higher amygdala BDNF response. Also, enriched animals showed higher brain weight compared to isolation reared rats as well as higher testis weight and hematocrit value compared to animals reared in standard laboratory condition. Rats showed less body weights in isolated condition. In conclusion, the BDNF profile of enriched animals might represent the neurobiological correlate of resilience phenotype under a stressful situation.

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The gut-microbiota–brain axis plays an important role in stress-related disorders, and dysfunction of this complex bidirectional system is associated with Alzheimer’s disease. This study aimed to assess the idea that whether gut microbiota depletion from early adolescence can alter anxiety- and depression-related behaviours in adult mice with or without Alzheimer-like disease. Male C57BL/6 mice were treated with an antibiotic cocktail from weaning to adulthood. Adult mice received an intracerebroventricular injection of amyloid-beta (Aβ)1–42, and were subjected to anxiety and depression tests. We measured, brain malondialdehyde and glutathione following anxiety tests, and assessed brain oxytocin and the hypothalamic–pituitary–adrenal (HPA) axis function by measuring adrenocorticotrophic hormone (ACTH) and corticosterone following depression tests. Healthy antibiotic-treated mice displayed significant decreases in anxiety-like behaviours, whereas they did not show any alterations in depression-like behaviours and HPA axis function. Antibiotic treatment from early adolescence prevented the development of anxiety- and depression-related behaviours, oxidative stress and HPA axis dysregulation in Alzheimer-induced mice. Antibiotic treatment increased oxytocin in the brain of healthy but not Alzheimer-induced mice. Taken together, these findings suggest that gut microbiota depletion following antibiotic treatment from early adolescence might profoundly affect anxiety- and depression-related behaviours, and HPA axis function in adult mice with Alzheimer-like disease.

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