Power AE, Thal LJ, McGaugh JL (2001) Memory enhancement induced by post-training norepinephrine in the basolateral amygdala is blocked by 192-IgG saporin lesions of the nucleus basalis magnocellularis. Neuroscience 2001 Abstracts 84.13. Society for Neuroscience, San Diego, CA.
Summary: Drugs and stress hormones act in the basolateral amygdala (BLA) to modulate memory storage. The BLA projects to the nucleus basalis magnocellaris (NBM), which sends broad cholinergic projections to the neocortex. These NBM-cortex projections have been implicated in learning, memory storage and cortical plasticity. The current study was designed to test whether the cholingeric NBM-cortex projections are involved in BLA-mediated memory modulation. Rats were given bilateral cholinergic lesions of the NBM with 192-IgG saporin (0.1 μg/ 0.5 μl per side) or sham infusions, and implanted with bilateral cannulae aimed at the BLA. One week after surgery the rats were trained in the inhibitory avoidance task. Immediately after training, the rats were given bilateral infusions of norepinephrine (0.3μg, 1.0 μg, or 3.0 μg) or vehicle (0.2 μl PBS) into the BLA. On a 48-h retention test, the norepinephrine infusions produced a dose-dependent enhancement of retention (0.3μg and 1.0 μg doses) in sham-operated controls. NBM-lesioned rats that received these memory-enhancing doses of norepinephrine had retention latencies that did not differ from vehicle infused controls. Thus memory enhancement induced by post-training intra-BLA infusion of norepinephrine was blocked in 192-IgG saporin NBM-lesioned rats. ChAT assays of frontal and occipital cortices confirmed the lesions. These findings indicate that the cholinergic NBM-cortex projections are involved in BLA-mediated modulation of memory.
Related Products: 192-IgG-SAP (Cat. #IT-01)