Once consolidated, a long-term memory item could regain susceptibility to consolidation blockers, that is, reconsolidate, upon its reactivation. Both consolidation and reconsolidation require protein synthesis, but it is not yet known how similar these processes are in terms of molecular, cellular, and neural circuit mechanisms. Whereas most previous studies focused on aversive conditioning in the amygdala and the hippocampus, here we examine the role of the ventromedial prefrontal cortex (vmPFC) in consolidation and reconsolidation of object recognition memory. Object recognition memory is the ability to discriminate the familiarity of previously encountered objects. We found that microinfusion of the protein synthesis inhibitor anisomycin or the N-methyl-D-aspartate (NMDA) receptor antagonist D,L-2-amino-5-phosphonovaleric acid (APV) into the vmPFC, immediately after training, resulted in impairment of long-term (24 h) but not short-term (3 h) recognition memory. Similarly, microinfusion of anisomycin or APV into the vmPFC immediately after reactivation of the long-term memory impaired recognition memory 24 h, but not 3 h, post-reactivation. These results indicate that both protein synthesis and NMDA receptors are required for consolidation and reconsolidation of recognition memory in the vmPFC.
Bibliographical noteFunding Information:
This work was supported by a grant from The National Institute for Psychobiology in Israel (number 22-2004-5) to MM and by The Ebelin and Gerd Bucerius ZEIT Foundation to MM and by a grant from The National Institute for Psychobiology in Israel to IA. We thank Prof. Yadin Dudai from the Department of Neurobiology at the Weizmann Institute of Science in Rehovot for the helpful comments on this paper and for the technical assistance provided by his laboratory. We also thank Dr Dan Yaniv for helpful comments on this paper.
- Object recognition memory
- Ventromedial prefrontal cortex
ASJC Scopus subject areas
- Cognitive Neuroscience
- Cellular and Molecular Neuroscience