Fig. 4

Hippocampal Nlrp1a knockdown rescues CSDS-induced autophagy impairment and depressive-like behavior in mice. A Scheme of AAV–shRNA infusion, social defeat stress and behavior test. B Hippocampal immunofluorescence image and representative immunoreactive bands showing the knockdown efficacy of AAV–Nlrp1a–shRNA. C–H Representative immunoreactive bands (C) and statistical results show that hippocampal Nlrp1a knockdown reversed CSDS-induced decrease in the expression of LC3-II/LC3-I (D), Beclin-1 (E), Atg5 (F), Atg7 (G) and increase in the expression of p62 (H). n = 6. I, J Representative images (I) and statistical results (J) show that hippocampal Nlrp1a knockdown inhibited CSDS-induced decrease in the number of autophagosomes (arrow). n = 3. Scale bar = 500 nm. K–M Representative immunoreactive bands and statistical results show that hippocampal Nlrp1a knockdown prevented CSDS-induced increase in the expression of p-PI3K (K), p-AKT (L) and p-mTOR (M). N, O Representative traces and statistical results show that hippocampal Nlrp1a knockdown increased the total moving distance (N) and the social interaction (O) in depressive-like mice. P Statistical results show that hippocampal Nlrp1a knockdown increased the sucrose preference in depressive-like mice. n = 6. Data were expressed as means ± SEM, *p < 0.05, **p < 0.01 vs. control group or CSDS group