Recovery as a function of the degree of amnesia due to protein synthesis inhibition.
Retrograde amnesia following inhibition of cerebral protein synthesis has generally been explained as either a failure of consolidation or impairment of a retrieval mechanism. Major evidence for the retrieval hypothesis is provided by studies which utilize a reminder (usually footshock) to attenuate the effect of the protein inhibitor. To examine this question, mice were injected subcutaneously with anisomycin (1 mg/animal, 7 mg/animal, or 1 mg/animal every 2 hr x 7) and given one training trial in a passive avoidance box. All animals received a single retention test on each of four consecutive days, starting either 1, 7, or 21 days after training. One-half of the mice in each group received a footshock reminder 1 hr after their initial test. The footshock reminder did not attenuate the inhibitor-induced amnesia, but multiple testing did produce partial recovery in animals demonstrating some memory of training (both Saline and Anisomycin animals). Animals injected with anisomycin whose testing began 1 day after training demonstrated partial recovery irrespective of drug dosage level. The extent of amnesia and recovery were dependent upon both drug dosage and training-test interval. Implications for the consolidation and retrieval hypotheses are discussed.
D000647:Amnesia / Q000139:chemically induced / Q000503:physiopathology*; D000818:Animals; D000841:Anisomycin / Q000494:pharmacology; D001921:Brain / Q000187:drug effects / Q000378:metabolism*; D003216:Conditioning, Operant / Q000187:drug effects; D004597:Electroshock; D006801:Humans; D008297:Male; D051379:Mice; D009419:Nerve Tissue Proteins / Q000096:biosynthesis / Q000502:physiology*; D013997:Time Factors
D009419:Nerve Tissue Proteins; D000841:Anisomycin