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. 2010 Feb 16;151(4):1795–1805. doi: 10.1210/en.2009-1026

Figure 4.

Figure 4

SL and LL rats exhibit distinct differences in novel restraint- and CRF-induced HPA response but not in dexamethasone-induced negative feedback. A, LL rats (n = 8) exhibited a facilitated response to restraint with higher ACTH at 15 min compared with SL rats (n = 7) and higher ACTH at 30 min compared with both SL and control rats (n = 9). In addition, SL rats exhibited significantly lower ACTH compared with controls at 30 min. B, Restraint-induced increases in corticosterone release were similar in SL (n = 5) and LL (n = 9) rats compared with controls (n = 10). C, Intravenous CRF (0.03 μg/kg) stimulated robust ACTH release in control (n = 7) and SL rats (n = 6) above that of vehicle treatment, whereas CRF (n = 7) was ineffective in stimulating ACTH release above that of vehicle-treated LL rats (n = 6). However, CRF-induced ACTH release was decreased in both SL and LL defeated rats compared with controls. D, Rats were treated with vehicle or dexamethasone (DEX, 0.03 mg/kg) 90 min before restraint stress. Compared with vehicle treatments (n = 6–9), dexamethasone blunted restraint-induced ACTH in control (n = 8), SL (n = 5), and LL (n = 7) rats. The dexamethasone suppression of restraint-induced ACTH release was consistent across groups. Average defeat latencies (seconds ± se) for rats in the novel restraint study (A and B) were 190 ± 21 and 415 ± 17 (P < 0.0001) for SL and LL rats, respectively. Average defeat latencies (seconds ± se) for rats in the CRF challenge study (C) were 261 ± 32 (SL, vehicle) and 558 ± 33 (LL, vehicle) (P = 0.0024) and 204 ± 67 (SL, CRF) and 521 ± 58 (LL, CRF) (P = 0.014). Latencies (seconds ± se) for rats in the dexamethasone challenge (D) were 225 ± 39 (SL, vehicle) and 559 ± 37 (LL, vehicle) (P < 0.0001) and 287 ± 40 (SL, DEX) and 574 ± 40 (LL, DEX) (P = 0.003). *, P < 0.05; **, P < 0.01; ***, P < 0.001, Bonferroni post hoc vs. vehicle treatment.