ABSTRACT
'New' memories are initially labile and sensitive to disruption before being consolidated into stable long-term memories. Much evidence indicates that this consolidation involves the synthesis of new proteins in neurons. The lateral and basal nuclei of the amygdala (LBA) are believed to be a site of memory storage in fear learning. Infusion of the protein synthesis inhibitor anisomycin into the LBA shortly after training prevents consolidation of fear memories. Here we show that consolidated fear memories, when reactivated during retrieval, return to a labile state in which infusion of anisomycin shortly after memory reactivation produces amnesia on later tests, regardless of whether reactivation was performed 1 or 14 days after conditioning. The same treatment with anisomycin, in the absence of memory reactivation, left memory intact. Consistent with a time-limited role for protein synthesis production in consolidation, delay of the infusion until six hours after memory reactivation produced no amnesia. Our data show that consolidated fear memories, when reactivated, return to a labile state that requires de novo protein synthesis for reconsolidation. These findings are not predicted by traditional theories of memory consolidation.
Subject(s)
Amygdala/physiology , Fear , Memory/physiology , Nerve Tissue Proteins/physiology , Amnesia/chemically induced , Amygdala/metabolism , Animals , Anisomycin/pharmacology , Conditioning, Classical , Electroshock , Male , Mental Recall/physiology , Nerve Tissue Proteins/biosynthesis , Protein Synthesis Inhibitors/pharmacology , Rats , Rats, Sprague-DawleyABSTRACT
The role of the sympathetic nervous system in generating behaviourally linked blood pressure (BP) responses was investigated in awake rats instrumented for chronic intra-arterial BP recording. All data from the recording sessions were digitalized and processed by a computer. Frequency interval histograms of behaviourally associated changes of BP and heart rate (HR) were generated. 6-Hydroxydopamine (100 and 200 mg/kg intravenously) was used for chemosympathectomy. In the intact rats (n = 8) three different frequency histograms of mean BP values for three behavioural groupings were generated (from lowest to highest average values): (1) resting, (2) exploring-grooming and (3) eating-drinking. Chemosympathectomy (n = 5) abolished this order of BP changes; mean BP did not rise from rest to other behaviours, nor did it vary during different behaviours. It is concluded that the sympathetic nervous system is responsible for producing the changes in BP that are appropriate and characteristic of each behaviour in awake, unrestrained rats.
