Article Figures & Data
Figures
- Fig. 1.
Extent of hippocampal lesion. A,B, Typical brain sections from the control group (A) and the hippocampal-lesion group (B). Sections of 40 μm were stained with cresyl violet. Scale bars, 1 mm. C, D, Histological reconstruction of the control group (C) and the hippocampal-lesion group (D). The filled andshaded areas indicate the least and the most extensive lesions, respectively. Numbers on theleft indicate stereotaxic coordinates (in millimeters) relative to bregma.
- Fig. 2.
Effect of hippocampal lesions made before conditioning. A, B, CR% in wild-type (A) and GluRδ2−/−(B) mice. These mice received a bilateral aspiration of the dorsal hippocampus and the overlying neocortex (hippocampal-lesion; filled circles;n = 7 for wild-type mice and n= 8 for mutant mice) or only the overlying neocortex (cortical-lesion;open circles; n = 8 for wild-type mice and n = 9 for mutant mice). C, CR% of the individual mice in the hippocampal-lesioned GluRδ2−/− sample. Each linerepresents the CR% of the individual mice. D, Temporal pattern of the CR in GluRδ2−/− mice. The EMG amplitude data in the last session were averaged and normalized by the activities before the CS in GluRδ2−/− mice. Thethin, thick, and dotted traces represent the control group, learned hippocampal-lesioned group, and nonlearned hippocampal-lesioned group, respectively. The horizontal lines at thebottom indicate the timing of the CS.
- Fig. 3.
Effect of hippocampal lesions made after 7 d of conditioning. A, B, CR% in wild-type (A) and GluRδ2−/−(B) mice. Mice were conditioned using a trace 0 paradigm for 7 d (1–7) and then on the next day received a hippocampal lesion (filled circles; n = 8 for wild-type mice andn = 7 for mutant mice) or a cortical lesion (open circles; n = 8 for wild-type mice and n = 8 for mutant mice). After 2 weeks of recovery, the mice were conditioned again for an additional 7 d (p1–p7). C, Retention index of the CR after the lesion. The ratio of the CR% in the first postlesion session to that in the last prelesion session was calculated for wild-type mice (wt) and for mutant mice (d2). c and h refer to cortical lesion and hippocampal lesion, respectively. D, The temporal pattern of the CR in the first postlesion session of GluRδ2−/− mice. The thin andthick traces represent the control group and hippocampal-lesioned group, respectively.
- Fig. 4.
Effect of hippocampal lesions made immediately after conditioning. A, B, CR% in wild-type (A) and GluRδ2−/− (B) mice. Mice were conditioned until their CR% exceeded 70% and on the next day received a hippocampal lesion (filled circle;n = 9 for wild-type mice and n= 8 for mutant mice) or a cortical lesion (open circle;n = 8 for wild-type mice and n= 7 for mutant mice). −1 and p1–p7represent the last prelesion session and the postlesion sessions, respectively. C, D, CR% of the individual mice in the cortical-lesioned GluRδ2−/− mice (C) and hippocampal-lesioned GluRδ2−/− mice (D). Each line represents the CR% of the individual mice. E, Retention index (see Fig.3C) of the CR after the lesion. c andh refer to cortical lesion and hippocampal lesion, respectively. F, The temporal pattern of the CR in the first postlesion session of GluRδ2−/− mice. Thethin and thick traces represent the control group and hippocampal-lesioned group, respectively.
