Amygdala or hippocampus inactivation after retrieval induces temporary memory deficit

Neurobiol Learn Mem. 2006 Sep;86(2):144-9. doi: 10.1016/j.nlm.2006.01.006. Epub 2006 Mar 15.

Abstract

The hypothesis that memory is stored through a single stage of consolidation that results in a stable and lasting long-term memory has been challenged by the proposition that reactivation of a memory induces reconsolidation of the memory. The reconsolidation hypothesis is supported by evidence that, under some conditions, post-retrieval treatments affecting amygdala and hippocampus functioning impair subsequent retention performance. We now report that repeated retention testing attenuates the performance impairment induced by post-retrieval reversible inactivation of the amygdala and hippocampus of rats induced by tetrodotoxin. These findings challenge the reconsolidation hypothesis and suggest that the post-retrieval retention performance impairment is best explained as due to temporary retrieval failure.

Publication types

  • Comparative Study
  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Action Potentials / drug effects
  • Action Potentials / physiology
  • Amnesia, Retrograde / chemically induced*
  • Amygdala / drug effects*
  • Amygdala / physiology
  • Animals
  • Avoidance Learning / drug effects
  • Avoidance Learning / physiology
  • Dose-Response Relationship, Drug
  • Hippocampus / drug effects*
  • Hippocampus / physiology
  • Male
  • Microinjections
  • Rats
  • Rats, Wistar
  • Retention, Psychology / drug effects*
  • Retention, Psychology / physiology
  • Sodium Channel Blockers / administration & dosage
  • Tetrodotoxin / administration & dosage*
  • Time Factors

Substances

  • Sodium Channel Blockers
  • Tetrodotoxin