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Lesion of the lateral entorhinal cortex amplifies odor‐induced expression of c‐fos , junB , and zif 268 mRNA in rat brain
Author(s) -
Bernabeu Ramón,
Thiriet Nathalie,
Zwiller Jean,
Di Scala Georges
Publication year - 2005
Publication title -
synapse
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.809
H-Index - 106
eISSN - 1098-2396
pISSN - 0887-4476
DOI - 10.1002/syn.20224
Subject(s) - piriform cortex , olfactory bulb , entorhinal cortex , junb , neuroscience , olfactory system , anterior olfactory nucleus , odor , subiculum , c fos , amygdala , hippocampus , immediate early gene , lesion , olfactory tubercle , stimulation , cortex (anatomy) , central nervous system , biology , psychology , gene expression , dentate gyrus , gene , biochemistry , psychiatry
Paradoxical facilitation of olfactory learning following entorhinal cortex (EC) lesion has been described, which may result from widespread functional alterations taking place within the olfactory system. To test this hypothesis, expression of the immediate early genes c‐fos , junB , and zif 268 was studied in response to an olfactory stimulation in several brain areas in control and in EC‐lesioned rats. Olfactory stimulation in control rats induced the expression of the three genes in the granular/mitral and glomerular layers of the olfactory bulb, as well as c‐fos and junB expression in the piriform cortex. However EC lesion was devoid of effects in nonstimulated animals; it significantly amplified the odor‐induced expression of the three genes in these areas, as well as in the amygdala, hippocampus, and parietal‐temporal cortices. The data suggest that EC lesion modifies the neural processing of odor by suppressing an inhibitory influence on brain areas connected to this cortex. Synapse 59:135–143, 2006. © 2005 Wiley‐Liss, Inc.