Fig. 3

PGRN deficiency in the NAc plays an antidepressant role in the NAc LPS challenge-induced depressive-like phenotype. A Graphical depiction of the experimental timeline in depression-like relevant behavioral tests after NAc LPS challenge in the WT and PGRNKO mice. B Sucrose preference between WT saline-control mice and PGRNKO saline-control mice had no obvious changes. PGRN deficiency in mice attenuated the decreased of sucrose preference induced by NAc LPS exposure, compared to NAc LPS-treated WT mice. NAc Pretreatment with recombinant PGRN decreased the sucrose preference increased in the PGRNKO mice after NAc LPS injection, compared to control group. C Immobility time of TST in NAc saline-treated PGRNKO mice was marked less than that of NAc saline-treated WT mice. NAc LPS exposure-induced TST immobility increased was reversed in the PGRNKO mice, while recombinant PGRN pretreatment enhanced the decreased in TST immobility in the PGRNKO mice after NAc LPS injection. D There are no significant in FST immobility between WT saline-treated and PGRN saline-treated mice. But, PGRN deficiency in mice reversed the NAc LPS challenge-induced an increase of FST immobility relative to NAc LPS-treated WT mice. Recombinant PGRN injection into NAc significantly elevated the decreased in the FST immobility from PGRNKO mice during NAc LPS exposure, compared to control group. FST: forced swim test, TST: tail suspension test. n = 10–12 per group. Data were analyzed by one-way ANOVA followed by the LSD multiple comparisons test, and expressed as mean ± SEM. **p < 0.01, ***p < 0.001, ns not significant