Recovery as a function of the degree of amnesia due to protein synthesis inhibition

Pharmacol Biochem Behav. 1978 Jun;8(6):701-10. doi: 10.1016/0091-3057(78)90269-1.

Abstract

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.

Publication types

  • Research Support, U.S. Gov't, Non-P.H.S.
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Amnesia / chemically induced
  • Amnesia / physiopathology*
  • Animals
  • Anisomycin / pharmacology
  • Brain / drug effects
  • Brain / metabolism*
  • Conditioning, Operant / drug effects
  • Electroshock
  • Humans
  • Male
  • Mice
  • Nerve Tissue Proteins / biosynthesis
  • Nerve Tissue Proteins / physiology*
  • Time Factors

Substances

  • Nerve Tissue Proteins
  • Anisomycin