Figure 3
From: Uncoupling DAPK1 from NMDA receptor GluN2B subunit exerts rapid antidepressant-like effects
GluN2B-specific antagonist produced rapid antidepressant-like effects and reversed CUS-induced synaptic protein deficits. (a) Timeline of CUS exposure, ifenprodil administration and behavioral testing (n=8–9 per group). (b, c) Acute ifenprodil administration dose-dependently increased sucrose preference in the SPT (b) and reduced immobility time in the FST (c) in CUS-exposed rats. (d) Timeline of CUS exposure, ifenprodil injection and decapitation (n=8–10 per group). (e) Representative western blots and quantification of fold changes in GluN1, GluN2A, p-GluN2A, GluN2B, p-GluN2B, DAPK1, CREB, p-CREB and BDNF in the mPFC 30 min, 1 h and 6 h after ifenprodil administration. (f) Timeline of CUS exposure, ifenprodil injection and decapitation (n=8–9 per group). (g) Representative western blots and quantification of fold changes in GluA1, synapsin I and PSD95 in synaptoneurosomes in the mPFC 6 h after ifenprodil administration. The data are expressed as mean±s.e.m. *P<0.05, **P<0.01, compared with control or control+vehicle group; #P<0.05, ##P<0.01, compared with CUS+vehicle group; n.s., nonsignificant difference. BDNF, brain-derived neurotrophic factor; CREB, cyclic AMP response element-binding protein; CUS, chronic unpredictable stress; DAPK1, death-associated protein kinase 1; FST, forced swim test; mPFC, medial prefrontal cortex; PSD95, postsynaptic density 95; SPT, sucrose preference test.
