From learning to forgetting: behavioral, circuitry, and molecular properties define the different functional states of the recognition memory trace.
Neuropsychological analyses of amnesic patients, as well as lesion experiments, indicate that the temporal lobe is essential for the encoding, storage, and expression of object recognition memory (ORM). However, temporal lobe structures directly involved in the consolidation and reconsolidation of these memories are not yet well-defined. We report here that systemic administration of a protein synthesis inhibitor before or up to 4 h after training or reactivation sessions impairs consolidation and reconsolidation of ORM, without affecting short-term memory. We have also observed that ORM reconsolidation is sensitive to protein synthesis inhibition, independently of the ORM trace age. Using bdnf and egr-1 gene expression analysis, we defined temporal lobe areas related to consolidation and reconsolidation of ORM. Training and reactivation 21 days after ORM acquisition sessions provoked changes in bdnf mRNA in somatosensory, perirhinal, and hippocampal cortices. Reactivation 2 days after the training session elicited changes in bdnf and egr-1 mRNA in entorhinal and prefrontal cortices, while reactivation 9 days post-training provoked an increase in egr-1 transcription in somatosensory and entorhinal cortices. The differences in activated circuits and in the capacity to recall the memory trace after 9 or 21 days post-training suggest that memory trace suffers functional changes in this period of time. All these results indicate that the functional state of the recognition memory trace, from acquisition to forgetting, can be specifically defined by behavioral, circuitry, and molecular properties.
Romero-Granados
Rocío
R
División de Neurociencias, Universidad Pablo de Olavide de Sevilla, Carretera de Utrera, Km. 1, 41013-Sevilla, Spain.
Fontán-Lozano
Angela
A
Delgado-García
José María
JM
Carrión
Angel M
AM
D015761:4-Aminopyridine / Q000494:pharmacology; D000367:Age Factors; D000818:Animals; D000841:Anisomycin / Q000494:pharmacology; D001522:Behavior, Animal / Q000187:drug effects / Q000502:physiology; D001921:Brain / Q000033:anatomy & histology / Q000187:drug effects / Q000378:metabolism*; D019208:Brain-Derived Neurotrophic Factor / Q000235:genetics / Q000378:metabolism; D004193:Discrimination Learning / Q000187:drug effects / Q000502:physiology*; D051766:Early Growth Response Protein 1 / Q000235:genetics / Q000378:metabolism; D005106:Exploratory Behavior / Q000187:drug effects / Q000502:physiology*; D005786:Gene Expression Regulation / Q000187:drug effects / Q000502:physiology*; D007093:Imidazoles; D008297:Male; D008569:Memory Disorders / Q000139:chemically induced / Q000473:pathology / Q000503:physiopathology*; D051379:Mice; D008810:Mice, Inbred C57BL; D009434:Neural Pathways / Q000187:drug effects / Q000378:metabolism; D026902:Potassium Channel Blockers / Q000494:pharmacology; D011500:Protein Synthesis Inhibitors / Q000494:pharmacology; D016760:Proto-Oncogene Proteins c-fos / Q000235:genetics / Q000378:metabolism; D011725:Pyridines; D012333:RNA, Messenger / Q000378:metabolism; D021641:Recognition, Psychology / Q000187:drug effects / Q000502:physiology*; D013997:Time Factors
C117326:57G709; D019208:Brain-Derived Neurotrophic Factor; D051766:Early Growth Response Protein 1; C486109:Egr1 protein, mouse; D007093:Imidazoles; D026902:Potassium Channel Blockers; D011500:Protein Synthesis Inhibitors; D016760:Proto-Oncogene Proteins c-fos; D011725:Pyridines; D012333:RNA, Messenger; D000841:Anisomycin; D015761:4-Aminopyridine