The Entorhinal Cortex-Nucleus Accumbens Pathway and Latent Inhibition: A Behavioral and Neurochemical Study in Rats

Latent inhibition (LI) refers to the decrease in conditioned response produced by the repeated nonreinforced preexposure to the to-be-conditioned stimulus. Experiment 1 investigated the effects of electrolytic lesions of the entorhinal cortex on LI in a conditioned emotional response procedure. Ento...

Full description

Saved in:
Bibliographic Details
Published in:Behavioral neuroscience 2002-02, Vol.116 (1), p.95-104
Main Authors: Coutureau, Etienne, Léna, Isabelle, Daugé, Valérie, Di Scala, Georges
Format: Article
Language:English
Subjects:
Animal
Animal behavior
Animals
Arousal - physiology
Biochemistry
Biological and medical sciences
Cerebral Cortex
Conditioning, Classical - physiology
Dopamine - physiology
Emotional Responses
Entorhinal Cortex
Entorhinal Cortex - physiology
Fear - physiology
Latent Inhibition
Male
Mental Recall - physiology
Motor Activity - physiology
Neural Inhibition - physiology
Neural Pathways - physiology
Neurology
Nucleus Accumbens - physiology
Rats
Rats, Long-Evans
Rodents
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Latent inhibition (LI) refers to the decrease in conditioned response produced by the repeated nonreinforced preexposure to the to-be-conditioned stimulus. Experiment 1 investigated the effects of electrolytic lesions of the entorhinal cortex on LI in a conditioned emotional response procedure. Entorhinal cortex lesions attenuated LI. Experiments 2 and 3 investigated whether this attenuation of LI could result from a modification in nucleus accumbens (NAcc) dopamine (DA) release. Rats with entorhinal cortex lesions displayed normal spontaneous and amphetamine-induced locomotor activity, as well as normal basal and amphetamine-induced release of DA within the NAcc (assessed by microdialysis). Taken together, these results show that entorhinal cortex lesions disrupt LI in a way that is unlikely to be due to an alteration of DA release within the NAcc.
ISSN:0735-7044
1939-0084
DOI:10.1037/0735-7044.116.1.95