Selective Involvement of the Lateral Entorhinal Cortex in the Control of the Olfactory Memory Trace During Conditioned Odor Aversion in the Rat

Evidence from the effect of aspiration lesions of the entorhinal cortex (EC) has shown that this region is involved in conditioned odor-aversion (COA) learning-that is, the avoidance of an odorized tasteless solution the ingestion of which precedes toxicosis-by rendering COA tolerant to long odor-to...

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Bibliographic Details
Published in:Behavioral neuroscience 2006-10, Vol.120 (5), p.1180-1186
Main Authors: Ferry, Barbara, Ferreira, Guillaume, Traissard, Natalia, Majchrzak, Monique
Format: Article
Language:English
Subjects:
Anatomical correlates of behavior
Animal
Animal memory
Animals
Association Learning - physiology
Aversion Conditioning
Avoidance Learning - physiology
Behavioral psychophysiology
Biological and medical sciences
Brain
Brain Mapping
Cerebral Cortex
Computer Science
Conditioning, Classical
Dominance, Cerebral - physiology
Entorhinal Cortex
Entorhinal Cortex - physiology
Fundamental and applied biological sciences. Psychology
Learning
Learning. Memory
Life Sciences
Lithium Chloride - toxicity
Male
Memory
Memory Trace
Mental Recall - physiology
Neurotoxicity
Odors
Olfactory Perception
Psychology. Psychoanalysis. Psychiatry
Psychology. Psychophysiology
Rats
Retention (Psychology) - physiology
Rodents
Smell - physiology
Toxicity
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Summary:Evidence from the effect of aspiration lesions of the entorhinal cortex (EC) has shown that this region is involved in conditioned odor-aversion (COA) learning-that is, the avoidance of an odorized tasteless solution the ingestion of which precedes toxicosis-by rendering COA tolerant to long odor-toxicosis delay. The present study examined whether neurotoxic lesions restricted to the lateral or medial parts of the EC, in comparison with large aspiration lesions, were sufficient to produce this effect. Male Long-Evans rats received odor-intoxication pairing with either a short (5-min) or long (120-min) delay between the presentation of the odor and toxicosis. All groups, including sham-lesioned controls, showed COA at the 5-min odor-toxicosis delay interval, but only rats with lateral EC damage displayed COA at the longer delay. These data show that the lateral EC is part of the substrate involved in the control of the olfactory memory trace during COA.
ISSN:0735-7044
1939-0084
DOI:10.1037/0735-7044.120.5.1180