Anisomycin infusion in amygdala impairs consolidation of odor aversion memory.
Brain Research. 2008-10-01; 1236: 166-175
DOI: 10.1016/j.brainres.2008.07.123
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1. Brain Res. 2008 Oct 21;1236:166-75. doi: 10.1016/j.brainres.2008.07.123. Epub
2008 Aug 12.
Anisomycin infusion in amygdala impairs consolidation of odor aversion memory.
Desgranges B(1), Lévy F, Ferreira G.
Author information:
(1)Laboratoire de Comportement, Neurobiologie et Adaptation, UMR6175,
INRA-CNRS-Université de Tours-Haras Nationaux, F-37380 Nouzilly, France.
Conditioned odor aversion (COA) results from the association between a novel odor
and a delayed visceral illness. Basolateral amygdala is crucial for COA learning
but its importance in COA consolidation remains to be demonstrated. We
investigated whether infusion of anisomycin, a protein synthesis inhibitor, in
the basolateral amygdala impaired COA consolidation. COA was greatly impaired
when anisomycin was infused immediately before odor-malaise pairing, but not
between odor and malaise. This suggests that the formation of odor
representation, rather than malaise integration, within the amygdala has been
disrupted. Anisomycin infusion before acquisition did not affect short-term
memory (tested 4 h after odor-malaise pairing) but dramatically impaired
long-term COA memory (tested 3 days later). This indicates specific consolidation
impairment. Control experiments indicated that anisomycin infusion did not affect
amygdala functionality and olfactory perception and did not induce cell death in
the amygdala. Moreover, anisomycin treatment induced an important decrease
(65-70%) of LiCl-induced Fos protein expression in the basolateral and the
central nuclei of the amygdala but not in adjacent piriform cortex indicating a
reliable and localized protein synthesis inhibition. These findings suggest the
pivotal role of the basolateral amygdala, and possibly the central amygdala, in
COA memory consolidation.
DOI: 10.1016/j.brainres.2008.07.123
PMID: 18725214 [Indexed for MEDLINE]