Amygdala or hippocampus inactivation after retrieval induces temporary memory deficit.
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.
Institute of Neurobiology and FES-Iztacala, National University of Mexico, Mexico. prado@servidor.unam-mx
Roberto A
RA
Prado-Alcalá
Miguel A
MA
Díaz del Guante
María E
ME
Garín-Aguilar
Arnulfo
A
Díaz-Trujillo
Gina L
GL
Quirarte
James L
JL
McGaugh
D000200:Action Potentials / Q000187:drug effects / Q000502:physiology; D000648:Amnesia, Retrograde / Q000139:chemically induced*; D000679:Amygdala / Q000187:drug effects* / Q000502:physiology; D000818:Animals; D001362:Avoidance Learning / Q000187:drug effects / Q000502:physiology; D004305:Dose-Response Relationship, Drug; D006624:Hippocampus / Q000187:drug effects* / Q000502:physiology; D008297:Male; D008845:Microinjections; D051381:Rats; D017208:Rats, Wistar; D012153:Retention, Psychology / Q000187:drug effects* / Q000502:physiology; D026941:Sodium Channel Blockers / Q000008:administration & dosage; D013779:Tetrodotoxin / Q000008:administration & dosage*; D013997:Time Factors
D026941:Sodium Channel Blockers; D013779:Tetrodotoxin