66, P < 0.05) and a significant genotype �� social defeat stress interaction was observed (F1,31 = 9.09, P < 0.01); no differences among groups were found except for significantly decreased values in wt defeated compared with wt control mice (P < 0.01). In general, the occupation of the corners opposite to the interaction zone was significantly increased in defeated subjects (F1,32 = 9.14, P < 0.01) and a significant interaction test phase �� social defeat stress was detected (F1,32 = 6.62, P < 0.05), due to the significantly selleck products
longer duration observed in TrkB.T1 defeated subjects compared with respective controls during the ��aggressor phase�� of the test (P < 0.05) (Fig. 2a). Coherently, the average time spent by subjects in the interaction zone was significantly increased by the aggressor presence compared with the ��nonaggressor phase�� of the test (F1,32 = 8.01, P < 0.01�Cnot shown ), and significantly decreased by social defeat stress (F1,32 = 9.01, P < 0.01) (Fig. 2b). Significant interactions between test phase and social defeat stress (F1,32 = 12.26, P < 0.01) and test phase �� social defeat stress �� genotype (F1,32 = 4.05, P = 0.05) were also found. Specifically, the time spent in the interaction zone during the ��aggressor phase�� was significantly lower in TrkB.T1 defeated compared with TrkB.T1 control mice (P < 0.01). The total distance traveled was significantly less during the ��aggressor�� phase compared AZ191
with the ��nonaggressor�� phase (F1,32 = 37.61, P < 0.001�Cnot shown ); overall, TrkB.T1 mice covered a significantly longer distance than wt mice (F1,32 = 5.59, P < 0.05), although no significant differences could be detected at individual group level (Fig. 2c). TrkB.T1 mice expressed significantly reduced protein levels of BDNF compared with wt littermates in the hippocampus (F1,32 = 9.61, P < 0.01) (Fig. 3). No effect of social defeat stress was highlighted. Internal organs. Adrenal gland's size was significantly increased in defeated animals (F1,32 = 7.81, P < 0.01); spleen size was significantly decreased in TrkB.T1 mice (F1,32 = 5.62, P < 0.05); thymus weight tended to be decreased in TrkB.T1 subjects (F1,32 = selleck inhibitor
3.49, P = 0.07); seminal vesicle weight was significantly diminished by both genotype (F1,32 = 5.76, P < 0.05) and social defeat stress (F1,32 = 6.06, P < 0.05); testicle size tended to be increased in TrkB.T1 mice (F1,32 = 4.05, P = 0.05); abdominal fat amount was significantly increased in TrkB.T1 mice compared with wt (F1,32 = 5.87, P < 0.05) and significantly decreased in defeated subjects compared with controls (F1,32 = 10.04, P < 0.01); a significant interaction between genotype and social defeat stress was also highlighted (F1,32 = 4.67, P < 0.05): defeated wt mice abdominal fat was significantly diminished compared with wt controls (P < 0.01) as well as compared with TrkB.T1 defeated subjects (P < 0.05) (Table 3). Plasma metabolic hormone, cytokine, and chemokine levels.