Lesions of the nucleus basalis magnocellularis induced by 192 IgG-saporin block memory enhancement with posttraining norepinephrine in the basolateral amygdala - PubMed (original) (raw)

Lesions of the nucleus basalis magnocellularis induced by 192 IgG-saporin block memory enhancement with posttraining norepinephrine in the basolateral amygdala

Ann E Power et al. Proc Natl Acad Sci U S A. 2002.

Abstract

Extensive evidence indicates that drugs and stress hormones act in the basolateral amygdala (BLA) to modulate memory consolidation. The BLA projects to the nucleus basalis magnocellularis (NBM), which sends broad cholinergic projections to the neocortex. NBM-cortex projections have been implicated in learning, memory storage, and plasticity. The current study investigated whether the cholinergic NBM-cortex projections are involved in BLA-mediated modulation of memory consolidation. Bilateral cholinergic cell lesions of the NBM were induced in rats with infusions of 192 IgG-saporin (0.1 microg/0.5 microl per side). Additionally, cannulae were implanted bilaterally in the BLA. One week after surgery, the rats were trained in an inhibitory avoidance task and, immediately after training, norepinephrine (0.3 microg, 1.0 microg, or 3.0 microg in 0.2 microl) or vehicle (PBS) was infused bilaterally into the BLA. Norepinephrine infusions produced a dose-dependent enhancement of 48-h retention (0.3 microg and 1.0 microg doses enhanced) in nonlesioned rats but did not affect retention in NBM-lesioned rats. Choline acetyltransferase assays of frontal and occipital cortices confirmed the NBM lesions. These findings indicate that cholinergic NBM-cortex projections are required for BLA-mediated modulation of memory consolidation.

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Figures

Figure 1

Figure 1

Only data from animals with posttraining infusion sites within the BLA were included in the analysis. (A) ♦ represents the infusion needle tip loci for a random sample of 30 rats included in the behavioral analysis. Coordinates indicate distance posterior to bregma. (B) Photomicrograph of a representative example of an infusion needle terminating within the BLA.

Figure 2

Figure 2

Intra-BLA infusions of norepinephrine immediately after IA training produce a dose-dependent enhancement of 48-h retention in sham-operated rats. The gray bar (tr.) indicates the mean training latency across all groups, which did not differ between any of the groups (P > 0.05). The mean training latency was significantly less than the retention latencies of the sham and lesion vehicle-infused groups (formula image, P < 0.05), which did not differ from each other (_P_ > 0.05). An ANOVA revealed significant main effects of the norepinephrine infusions, the 192 IgG-saporin lesion, and a significant norepinephrine infusion × lesion interaction effect (P < 0.05). The 0.3 μg (*, _P_ < 0.01) and the 1.0 μg (**, _P_ < 0.001) doses significantly enhanced retention relative to the vehicle-infused sham group. Rats with the 192 IgG-saporin NBM-lesions did not show memory enhancement with norepinephrine infusions. The mean retention latencies of the 0.3 μg (#, _P_ < 0.05) and the 1.0 μg (##, _P_ < 0.001) dose lesion groups were significantly shorter than those of their respective dose-matched sham control groups, but did not differ from that of the vehicle-infused sham or lesion groups (_P_ > 0.05). (The number of animals per group are as follows: sham-vehicle, 11; sham-norepinephrine 0.3 μg, 10; sham-norepinephrine 1.0 μg, 10; sham-norepinephrine 3.0 μg, 9; lesion-vehicle, 9; lesion-norepinephrine 0.3 μg, 7; lesion-norepinephrine 1.0 μg, 8; lesion-norepinephrine 3.0 μg, 14.)

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