Brain-derived neurotrophic factor (BDNF) and tyrosine kinase B (TrkB) have been implicated in depressive/anxiety disorders. The efficacy of antidepressants may be related to BDNF-TrkB signaling fueling neuroplastic changes. TrkB.T1 might have novel signaling effects that may be relevant for dealing with stressors. Using mice lacking TrkB.T1 exposed to chronic stress, we assessed behavioral and TrkB expression profiles, as well as gut-microbial profile. Our results showed that while repeated different stressor regimen did markedly alter open-field performance, this was unaffected by the TrkB.T1 knockout. A sex effect was apparent, however male mice showed the greatest exploration abnormalities. TrkB expression in amygdala varied as a function of sex; yet, there were no observed difference in the gut microbiota among the groups. These data do not support major role for TrkB.T1 in modulating anxiety, but there were many limitations of this thesis study. Further experiments will focus on the phenotype of TrkB.T1 mice.