Research Paper Volume 13, Issue 16 pp 20748—20761

Enriched environment remedies cognitive dysfunctions and synaptic plasticity through NMDAR-Ca2+-Activin A circuit in chronic cerebral hypoperfusion rats

EE induces ActA to promotes Ca2+ influx in CCH rats. (A) Immunofluorescence staining and Western blot were used to detect the expression of cognitive-related proteins. Levels of L-glutamate (GLU). (B, C) The content of Ca2+ in the cerebral cortex and hippocampus. Levels of NMDAR, NR2A, NR2B. (D) The content of ActA in the cerebral cortex and hippocampus. (E–G) Levels of Act A. The content of Ca2+ and ActA block with FSH in the cerebral cortex and hippocampus. Levels of NMDAR, NR2A, NR2B block with FSH in the cerebral cortex and hippocampus. *p #p N = 5. *p #p

Figure 3. EE induces ActA to promotes Ca2+ influx in CCH rats. (A) Immunofluorescence staining and Western blot were used to detect the expression of cognitive-related proteins. Levels of L-glutamate (GLU). (B, C) The content of Ca2+ in the cerebral cortex and hippocampus. Levels of NMDAR, NR2A, NR2B. (D) The content of ActA in the cerebral cortex and hippocampus. (EG) Levels of Act A. The content of Ca2+ and ActA block with FSH in the cerebral cortex and hippocampus. Levels of NMDAR, NR2A, NR2B block with FSH in the cerebral cortex and hippocampus. *p < 0.05, vs. Sham group; #p < 0.05, vs. CCH group. Sham group, treated with an equal volume of vehicle; CCH group, chronic cerebral hypoperfusion and no treatment; EE group, CCH and treated with EE. EEF group, CCH and treated with EE and FSH. N = 5. *p < 0.05, #p < 0.05.