Figure legends

Figure legends
Fig.1. CCL exposure impaired hippocampus-dependent spatial memory in the MWM task. (A) Locomotor activity rhythm was disrupted by CCL exposure in the open field test compared with CTL rats. (B) CCL rats showed shorter escape latency during training day 1 – 2. (C) CCL rats spent less time in the target quadrant in the retrieval test. (D) CCL exposure did not influence the visible platform learning.(E) CCL exposure did not influence working memory in the MWM. (F) Jumping behaviours/rat (jump back into the pool when they have escaped on the hidden platform during the training day). Data are mean ± SEM. * p < 0.05, ** p < 0.01 CCL vs.CTL rats.
Fig.2. CCL exposure reduced stress response. (A) CCL exposure reduced thigmotaxis behavior on training day 1 – 3 in the MWM compared with CTL rats. (B) CCL rats spent more time in the open arms than CTL rats in the elevated-plus maze test. (C) CCL rats made more frequent entries to open arm than CTL rats. Data are mean ±SEM. * p < 0.05, ** p < 0.01 CCL vs. CTL rats.
Fig.3. CCL exposure influenced hippocampal LTD. (A) CCL exposure failed to induce LTD measured 50 – 60 min after low frequency stimulation (LFS, bar, 1 Hz) (p > 0.05 vs. baseline),while short-term depression (within 30 min after LFS) was significantly smaller in CCL rats than in control rats (CCL vs. CTL). (B)Additional acute elevated platform stress enabled LFS to induce LTD in CTL but not in CCL rats (p < 0.01, CCL+EP vs. CTL+EP). All sample traces were taken 10 min after
commencement of baseline recording and 55 min after stimulation protocol. Calibration: 0.5 mV, 10 ms.
Fig.4. CCL exposure impaired L-LTP in the hippocampus CA1 region. (A)
Input–output curve for the fEPSP amplitude remained unchanged after CCL exposure. The stimulus intensity is controlled by Scope Software in mV to trigger a stimulus isolator to output the corresponding currents in mA. (B)E-LTP is similar between the CTL and CCL rats induced by 3 bursts of theta-burst stimulation (TBS). (C) 12 bursts of TBS evoked L-LTP in CCL slices (CCL, filled circles) that decayed to baseline after 3-h but evoked L-LTP in CTL slices (CTL, open circles) that endured for at least 3-h.
Fig.5. The role of D1/D5 receptors in CCL exposure induced impairment of L-LTP.
(A)Pairing 12 bursts of TBS with SCH23390 application rescues the impairment of
L-LTP in CCL rats (Sch, filled circles). (B)SCH23390 or SKF38393 application alone respectively has no long-lasting effects on synaptic strength. (C)Pairing 12 bursts of TBS with SKF38393 application further impaired L-LTP in CCL rats (Skf, filled circles). (D)Summary histogram. **p < 0.01, *p < 0.05 vs. CCL.
Fig.6. The role of D1/D5 receptors in L-LTP of CTL rats. (A)Pairing 12 bursts of TBS with SCH23390 (1μm) application impaired L-LTP in CTL rats (Sch, filled circles). (B)Pairing 3 bursts of TBS with SKF38393 (25μm) converts E-LTP to
L-LTP in CTL rats (Skf, filled circles).
Fig.7. CCL increased locomotor activity (means ± SEM) in an open field test. (A)CCL rats traveled a longer distance than CTL rats. **p < 0.01, CCL versus CTL rats. (B) Vertical rears in an open field. **p < 0.01 CCL versus CTL rats.。