Literature DB >> 2306613

Involvement of amygdala pathways in the influence of post-training intra-amygdala norepinephrine and peripheral epinephrine on memory storage.

K C Liang1, J L McGaugh, H Y Yao.   

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 (0.2 microgram) as well as the amnestic effect of a high dose of NE (5.0 microgram). In contrast, VAF transections did not block the memory-enhancing effect of NE (0.2 microgram). 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 influence 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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Year:  1990        PMID: 2306613     DOI: 10.1016/0006-8993(90)90400-6

Source DB:  PubMed          Journal:  Brain Res        ISSN: 0006-8993            Impact factor:   3.252


  52 in total

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9.  An emotion-induced retrograde amnesia in humans is amygdala- and beta-adrenergic-dependent.

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10.  Enhanced retention in the passive-avoidance task by 5-HT(1A) receptor blockade is not associated with increased activity of the central nucleus of the amygdala.

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