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Short Communication

Systemic and intrahippocampal administrations of the glucocorticoid receptor antagonist RU38486 impairs fear memory reconsolidation in rats

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Pages 459-464 | Received 13 Aug 2010, Accepted 10 Dec 2010, Published online: 27 Mar 2011

Figures & data

Figure 1.  (A) Diagrammatic representation of a histology section, redrawn from Paxinos and Watson (Citation2005). The dark irregular areas define the range of cannula tip locations within the dorsal hippocampus. (B) A representative photomicrograph of a coronal section, stained with cresyl violet, illustrating placement of cannula and injection needle tip (arrow) in the dorsal hippocampus. CA1, CA3, Ammon's horn; DG, dentate gyrus.

Figure 1.  (A) Diagrammatic representation of a histology section, redrawn from Paxinos and Watson (Citation2005). The dark irregular areas define the range of cannula tip locations within the dorsal hippocampus. (B) A representative photomicrograph of a coronal section, stained with cresyl violet, illustrating placement of cannula and injection needle tip (arrow) in the dorsal hippocampus. CA1, CA3, Ammon's horn; DG, dentate gyrus.

Figure 2.  Effects of RU38486 administration following memory reactivation on fear memory reconsolidation. (A) Passive avoidance training/testing and drug administration schedule; intervals are 2 or 7 days (d). (B) Median ( ± interquartile ranges) step-through retention latencies of groups of rats systemically injected with 20 mg/kg of RU38486 (n = 8) or vehicle (VEH; n = 8) immediately after Test 1 (T1) and re-tested 2 days (Test 2), 7 days (Test 3), and after a reminder shock (Test 4). (C) Median ( ± interquartile ranges) step-through latencies of groups of rats received intrahippocampal injections of RU38486 (0.3 or 3 ng) (n = 8 in each group) or VEH (n = 8) immediately after Test 1 and re-tested 2 days (Test 2) and 7 days (Test 3) later and after a reminder shock (Test 4). Latencies were significantly different between groups in all retention test sessions. (Mann–Whitney U-tests, two-tailed, *P = 0.0005 compared with the vehicle (VEH) group).

Figure 2.  Effects of RU38486 administration following memory reactivation on fear memory reconsolidation. (A) Passive avoidance training/testing and drug administration schedule; intervals are 2 or 7 days (d). (B) Median ( ± interquartile ranges) step-through retention latencies of groups of rats systemically injected with 20 mg/kg of RU38486 (n = 8) or vehicle (VEH; n = 8) immediately after Test 1 (T1) and re-tested 2 days (Test 2), 7 days (Test 3), and after a reminder shock (Test 4). (C) Median ( ± interquartile ranges) step-through latencies of groups of rats received intrahippocampal injections of RU38486 (0.3 or 3 ng) (n = 8 in each group) or VEH (n = 8) immediately after Test 1 and re-tested 2 days (Test 2) and 7 days (Test 3) later and after a reminder shock (Test 4). Latencies were significantly different between groups in all retention test sessions. (Mann–Whitney U-tests, two-tailed, *P = 0.0005 compared with the vehicle (VEH) group).

Figure 3.  Effects of RU38486 administration in the absence of memory reactivation on fear memory reconsolidation. (A) Passive avoidance training/testing and drug administration schedule; intervals are 2 days (d); NR, no memory reactivation. (B) Median (interquartile ranges) step-through latencies of groups of rats given systemic (20 mg/kg) or intrahippocampal (3 ng in 1 μl per side) injection of RU38486 or vehicle (VEH; n = 8) in the absence of memory reactivation and tested 2 days; VEH, vehicle.

Figure 3.  Effects of RU38486 administration in the absence of memory reactivation on fear memory reconsolidation. (A) Passive avoidance training/testing and drug administration schedule; intervals are 2 days (d); NR, no memory reactivation. (B) Median (interquartile ranges) step-through latencies of groups of rats given systemic (20 mg/kg) or intrahippocampal (3 ng in 1 μl per side) injection of RU38486 or vehicle (VEH; n = 8) in the absence of memory reactivation and tested 2 days; VEH, vehicle.

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