Spared anterograde memory for shock-probe fear conditioning after inactivation of the amygdala

Abstract

Previous studies have shown that amygdala lesions impair avoidance of an electrified probe. This finding has been interpreted as indicating that amygdala lesions reduce fear. It is unclear, however, whether amygdala-lesioned rats learn that the probe is associated with shock. If the lesions prevent the formation of this association, then pretraining reversible inactivation of the amygdala should impair both acquisition and retention performance. To test this hypothesis, the amygdala was inactivated (tetrodotoxin; TTX; 1 ng/side) before a shock-probe acquisition session, and retention was tested 4 d later. The data indicated that, compared with rats infused with vehicle, rats infused with TTX received more shocks during the acquisition session, but more importantly, were not impaired on the retention test. In Experiment 2, we assessed whether the spared memory on the retention test was caused by overtraining during acquisition. We used the same procedure as in Experiment 1, with the exception that the number of shocks the rats received during the acquisition session was limited to four. Again the data indicated that amygdala inactivation did not impair performance on the retention test. These results indicate that amygdala inactivation does not prevent the formation of an association between the shock and the probe and that shock-probe deficits during acquisition likely reflect the amygdala's involvement in other processes.

Figure 1

Illustrations of the infusion locations observed bilaterally through the rostral and caudal extent of the amygdala for the rats tested in Experiment 1. Atlas plates adapted from Paxinos and Watson (1997).

Figure 2

Photomicrograph of a coronal section of the temporal lobe showing a representative cannula placement (–2.8 mm relative to bregma; Paxinos and Watson 1997). Scale bar, 1.0 mm.

Figure 3

Mean (±SEM) number of contact-induced shocks received during the acquisition session by rats immediately pretreated with either VEHICLE or TTX into the amygdala. (*) p < 0.001 versus VEHICLE; n = 13–14 per group.

Figure 4

Mean (±SEM) (A) number of contact-induced shocks and (B) latency to the first contact-induced shock (retention latency) observed in rats that received pretraining intra-amygdala infusions of VEHICLE or TTX and were previously exposed to the electrified probe (SHOCK-EXPERIENCED) or not (SHOCK-NAIVE). (*) p < 0.01 versus VEHICLE-SHOCK-NAIVE; (▪) p < 0.01 versus TTX-SHOCK-NAIVE; n = 11–14 per group.

Figure 5

Illustrations of the infusion locations observed bilaterally through the rostral and caudal extent of the amygdala for the rats tested in Experiment 2. Atlas plates adapted from Paxinos and Watson (1997).

Figure 6

Mean (±SEM) (A) number of contact-induced shocks and (B), latency to the first contact-induced shock (retention latency) observed in rats that received pretraining intra-amygdala infusions of VEHICLE or TTX and were previously limited to four contacts with the electrified probe (SHOCK-EXPERIENCED) or the nonelectrified probe (SHOCK-NAIVE) during the acquisition session. (*) p < 0.05 versus VEHICLE-SHOCK-NAIVE; (▪) p < 0.05 versus TTX-SHOCK-NAIVE; n = 7–15 per group.