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Catecholaminergic depletion within the prelimbic medial prefrontal cortex enhances latent inhibition

Latent inhibition (LI) refers to the reduction in conditioning to a stimulus that has received repeated non-reinforced pre-exposure. Investigations into the neural substrates of LI have focused on the nucleus accumbens (NAc) and its inputs from the hippocampal formation and adjacent cortical areas....

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Detalles Bibliográficos
Autores principales: Nelson, A.J.D., Thur, K.E., Marsden, C.A., Cassaday, H.J.
Formato: Texto
Lenguaje:English
Publicado: Elsevier Science 2010
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2930211/
https://www.ncbi.nlm.nih.gov/pubmed/20619321
http://dx.doi.org/10.1016/j.neuroscience.2010.06.066
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author Nelson, A.J.D.
Thur, K.E.
Marsden, C.A.
Cassaday, H.J.
author_facet Nelson, A.J.D.
Thur, K.E.
Marsden, C.A.
Cassaday, H.J.
author_sort Nelson, A.J.D.
collection PubMed
description Latent inhibition (LI) refers to the reduction in conditioning to a stimulus that has received repeated non-reinforced pre-exposure. Investigations into the neural substrates of LI have focused on the nucleus accumbens (NAc) and its inputs from the hippocampal formation and adjacent cortical areas. Previous work has suggested that lesions to the medial prefrontal cortex (mPFC), another major source of input to the NAc, do not disrupt LI. However, a failure to observe disrupted LI does not preclude the possibility that a particular brain region is involved in the expression of LI. Moreover, the mPFC is a heterogeneous structure and there has been no investigation of a possible role of different regions within the mPFC in regulating LI under conditions that prevent LI in controls. Here, we tested whether 6-hydroxydopamine (6-OHDA)-induced lesions of dopamine (DA) terminals within the prelimbic (PL) and infralimbic (IL) mPFC would lead to the emergence of LI under conditions that do produce LI in controls (weak pre-exposure). LI was measured in a thirst motivated conditioned emotional response procedure with 10 pre-exposures to a noise conditioned stimulus (CS) and two conditioning trials. Sham-operated and IL-lesioned animals did not show LI and conditioned to the pre-exposed CS at comparable levels to the non-pre-exposed controls. 6-OHDA lesions to the PL, however, produced potentiation of LI. These results provide the first demonstration that the PL mPFC is a component of the neural circuitry underpinning LI.
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spelling pubmed-29302112010-09-20 Catecholaminergic depletion within the prelimbic medial prefrontal cortex enhances latent inhibition Nelson, A.J.D. Thur, K.E. Marsden, C.A. Cassaday, H.J. Neuroscience Cellular and Molecular Neuroscience Latent inhibition (LI) refers to the reduction in conditioning to a stimulus that has received repeated non-reinforced pre-exposure. Investigations into the neural substrates of LI have focused on the nucleus accumbens (NAc) and its inputs from the hippocampal formation and adjacent cortical areas. Previous work has suggested that lesions to the medial prefrontal cortex (mPFC), another major source of input to the NAc, do not disrupt LI. However, a failure to observe disrupted LI does not preclude the possibility that a particular brain region is involved in the expression of LI. Moreover, the mPFC is a heterogeneous structure and there has been no investigation of a possible role of different regions within the mPFC in regulating LI under conditions that prevent LI in controls. Here, we tested whether 6-hydroxydopamine (6-OHDA)-induced lesions of dopamine (DA) terminals within the prelimbic (PL) and infralimbic (IL) mPFC would lead to the emergence of LI under conditions that do produce LI in controls (weak pre-exposure). LI was measured in a thirst motivated conditioned emotional response procedure with 10 pre-exposures to a noise conditioned stimulus (CS) and two conditioning trials. Sham-operated and IL-lesioned animals did not show LI and conditioned to the pre-exposed CS at comparable levels to the non-pre-exposed controls. 6-OHDA lesions to the PL, however, produced potentiation of LI. These results provide the first demonstration that the PL mPFC is a component of the neural circuitry underpinning LI. Elsevier Science 2010-09-29 /pmc/articles/PMC2930211/ /pubmed/20619321 http://dx.doi.org/10.1016/j.neuroscience.2010.06.066 Text en © 2010 Elsevier Ltd. https://creativecommons.org/licenses/by/3.0/ Open Access under CC BY 3.0 (https://creativecommons.org/licenses/by/3.0/) license
spellingShingle Cellular and Molecular Neuroscience
Nelson, A.J.D.
Thur, K.E.
Marsden, C.A.
Cassaday, H.J.
Catecholaminergic depletion within the prelimbic medial prefrontal cortex enhances latent inhibition
title Catecholaminergic depletion within the prelimbic medial prefrontal cortex enhances latent inhibition
title_full Catecholaminergic depletion within the prelimbic medial prefrontal cortex enhances latent inhibition
title_fullStr Catecholaminergic depletion within the prelimbic medial prefrontal cortex enhances latent inhibition
title_full_unstemmed Catecholaminergic depletion within the prelimbic medial prefrontal cortex enhances latent inhibition
title_short Catecholaminergic depletion within the prelimbic medial prefrontal cortex enhances latent inhibition
title_sort catecholaminergic depletion within the prelimbic medial prefrontal cortex enhances latent inhibition
topic Cellular and Molecular Neuroscience
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2930211/
https://www.ncbi.nlm.nih.gov/pubmed/20619321
http://dx.doi.org/10.1016/j.neuroscience.2010.06.066
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