期刊
LEARNING & MEMORY
卷 13, 期 1, 页码 27-34出版社
COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
DOI: 10.1101/lm.91206
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资金
- NATIONAL INSTITUTE OF MENTAL HEALTH [R01MH012526, R37MH012526, R56MH012526] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [N01NS012333] Funding Source: NIH RePORTER
- NIMH NIH HHS [R56 MH012526, R01 MH012526, MH12526] Funding Source: Medline
- NINDS NIH HHS [N01NS12333] Funding Source: Medline
Recent studies have reported new evidence consistent with the hypothesis that reactivating a memory by re-exposure to a training context destabilizes the memory and induces reconsolidation. In the present experiments, rats' memory for inhibitory avoidance (1A) training was tested 6 h (Test 1), 2 d (Test 2), and 6 d (Test 3) after training. On Test 1 the rats were either removed from the shock compartment immediately after entry or retained in the shock context for 200 sec, and intrahippocarnpal infusions of the protein synthesis inhibitor anisomycin (75 mu g/side) were administered immediately after the test. Anisomycin infusions administered after Test 1 impaired 1A performance on Test 2 in animals given the brief re-exposure, but impaired extinction in animals exposed to the context for 200 sec. Rats with anisomycin-induced retention impairment on Test 2 demonstrated spontaneous recovery of retention performance on Test 3, whereas rats showing extinction on Test 2 showed further extinction on Test 3. The findings indicate that post-retrieval administration of anisomycin impairs subsequent retention performance only in the absence of extinction and that this impairment is temporary.
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