Abstract

These experiments examined the role of two major amygdala afferent-efferent pathways — the stria terminalis (ST) and the ventral amygdalofugal pathway (VAF) — in mediating the effects, on memory storage, of post-training intra-amygdala injections of norepinephrine (NE) and subcutaneous (s.c.) injections of epinephrine (E). Rats with either ST lesions or VAF transections and sham-operated rats were trained on a one-trial step-through inhibitory avoidance task and immediately after training received intra-amygdala injections of NE or a buffer solution. Other groups of VAF-transected animals received post-training s.c. injections of E or saline. ST lesions blocked the memory-enhancing effect of intra-amygdala injections of a low dose of NE (0.2μg) as well as the amnestic effect of a high dose of NE (5.0 μg). In contrast, VAF transections did not block the memory-enhancing effect of NE (0.2 μg). However, VAF transections attenuated the memory-enhancing effect of s.c. injections of E: the effective dose of E was shifted from 0.1 to 0.5 mg/kg. These findings, considered together with previous evidence that ST lesions block the memory-enhancing effect of peripheral E injections, suggest that the VAF is involved in mediating the central influences of peripheral E on amygdala functioning, while the ST is involved in mediating amygdala influences on memory storage elsewhere in the brain.

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