Abstract:
RATIONALE:In humans, the retrieval of memories associated with an alcohol-related experience frequently evokes alcohol-seeking behaviour. The reconsolidation hypothesis states that a consolidated memory could again become labile and susceptible to disruption after memory retrieval. OBJECTIVES:The aim of our study was to examine whether retrieval of alcohol-related memories undergoes a reconsolidation process. METHODS:For this purpose, male Wistar rats were trained to self-administer ethanol in the presence of specific conditioned stimuli. Thereafter, animals were left undisturbed in their home cages for the following 21 days. Memory retrieval was performed in a single 5-min exposure to all alcohol-associated stimuli. The protein synthesis inhibitor anisomycin, the non-competitive N-methyl-D: -aspartate (NMDA) receptor antagonist MK-801 and acamprosate, a clinically used drug known to reduce a hyper-glutamatergic state, were given immediately after retrieval of alcohol-related memories. The impact of drug treatment on cue-induced alcohol-seeking behaviour was measured on the following day and 7 days later. RESULTS:Administration of both anisomycin and MK-801 reduced cue-induced alcohol-seeking behaviour, showing that memory reconsolidation was disrupted by these compounds. However, acamprosate had no effect on the reconsolidation process, suggesting that this process is not dependent on a hyper-glutamatergic state but is more related to protein synthesis and NMDA receptor activity. CONCLUSIONS:Pharmacological disruption of reconsolidation of alcohol-associated memories can be achieved by the use of NMDA antagonists and protein synthesis inhibitors and may thus provide a potential new therapeutic strategy for the prevention of relapse in alcohol addiction.
journal_name
Psychopharmacology (Berl)journal_title
Psychopharmacologyauthors
von der Goltz C,Vengeliene V,Bilbao A,Perreau-Lenz S,Pawlak CR,Kiefer F,Spanagel Rdoi
10.1007/s00213-009-1544-1subject
Has Abstractpub_date
2009-08-01 00:00:00pages
389-97issue
3eissn
0033-3158issn
1432-2072journal_volume
205pub_type
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