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Enhanced training protects memory against amnesia produced by concurrent inactivation of amygdala and striatum, amygdala and substantia nigra, or striatum and substantia nigra
Memory is markedly impaired when normal activity of any of a number of cerebral structures is disturbed after a learning experience. A growing body of evidence indicates, however, that such interference with neuronal function becomes negligible when the learning experience is significantly enhanced....
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Frontiers Media S.A.
2011
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3243958/ https://www.ncbi.nlm.nih.gov/pubmed/22203796 http://dx.doi.org/10.3389/fnbeh.2011.00083 |
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author | Salado-Castillo, Rigoberto Sánchez-Alavéz, Manuel Quirarte, Gina L. Martínez García, María Isabel Prado-Alcalá, Roberto A. |
author_facet | Salado-Castillo, Rigoberto Sánchez-Alavéz, Manuel Quirarte, Gina L. Martínez García, María Isabel Prado-Alcalá, Roberto A. |
author_sort | Salado-Castillo, Rigoberto |
collection | PubMed |
description | Memory is markedly impaired when normal activity of any of a number of cerebral structures is disturbed after a learning experience. A growing body of evidence indicates, however, that such interference with neuronal function becomes negligible when the learning experience is significantly enhanced. We now report on the effects of enhanced training on retention after temporary inactivation of cerebral nuclei known to be involved in memory, namely the substantia nigra (SN), striatum (STR), and amygdala (AMY). When training was conducted with a relatively low intensity of footshock (1.0 mA), post-training infusion of lidocaine into the SN, STR, or AMY produced a marked memory deficit. Increasing the aversive stimulation to 2.0 mA protected memory from the amnesic effect of intranigral lidocaine, but there was still a deficit after its infusion into the STR and AMY. Administration of lidocaine into each of these nuclei, in the groups that had been trained with 3.0 mA, was completely ineffective in producing alterations in memory consolidation. Simultaneous infusion of lidocaine into STR + SN, AMY + SN, or AMY + STR was also ineffective in altering memory formation when the highest footshock intensity was used for training. To our knowledge, this is the first demonstration that an enhanced learning experience guards against memory deficits after simultaneous temporary interruption of neural activity of brain nuclei heretofore thought to be necessary for memory formation. These findings support the proposition that brain structures involved in memory processing are functionally connected in series during memory consolidation and that, after an enhanced learning experience, these structures become functionally connected in parallel. |
format | Online Article Text |
id | pubmed-3243958 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2011 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-32439582011-12-27 Enhanced training protects memory against amnesia produced by concurrent inactivation of amygdala and striatum, amygdala and substantia nigra, or striatum and substantia nigra Salado-Castillo, Rigoberto Sánchez-Alavéz, Manuel Quirarte, Gina L. Martínez García, María Isabel Prado-Alcalá, Roberto A. Front Behav Neurosci Neuroscience Memory is markedly impaired when normal activity of any of a number of cerebral structures is disturbed after a learning experience. A growing body of evidence indicates, however, that such interference with neuronal function becomes negligible when the learning experience is significantly enhanced. We now report on the effects of enhanced training on retention after temporary inactivation of cerebral nuclei known to be involved in memory, namely the substantia nigra (SN), striatum (STR), and amygdala (AMY). When training was conducted with a relatively low intensity of footshock (1.0 mA), post-training infusion of lidocaine into the SN, STR, or AMY produced a marked memory deficit. Increasing the aversive stimulation to 2.0 mA protected memory from the amnesic effect of intranigral lidocaine, but there was still a deficit after its infusion into the STR and AMY. Administration of lidocaine into each of these nuclei, in the groups that had been trained with 3.0 mA, was completely ineffective in producing alterations in memory consolidation. Simultaneous infusion of lidocaine into STR + SN, AMY + SN, or AMY + STR was also ineffective in altering memory formation when the highest footshock intensity was used for training. To our knowledge, this is the first demonstration that an enhanced learning experience guards against memory deficits after simultaneous temporary interruption of neural activity of brain nuclei heretofore thought to be necessary for memory formation. These findings support the proposition that brain structures involved in memory processing are functionally connected in series during memory consolidation and that, after an enhanced learning experience, these structures become functionally connected in parallel. Frontiers Media S.A. 2011-12-20 /pmc/articles/PMC3243958/ /pubmed/22203796 http://dx.doi.org/10.3389/fnbeh.2011.00083 Text en Copyright © 2011 Salado-Castillo, Sánchez-Alavez, Quirarte, Martínez García and Prado-Alcalá. http://www.frontiersin.org/licenseagreement This is an open-access article distributed under the terms of the Creative Commons Attribution Non Commercial License, which permits non-commercial use, distribution, and reproduction in other forums, provided the original authors and source are credited. |
spellingShingle | Neuroscience Salado-Castillo, Rigoberto Sánchez-Alavéz, Manuel Quirarte, Gina L. Martínez García, María Isabel Prado-Alcalá, Roberto A. Enhanced training protects memory against amnesia produced by concurrent inactivation of amygdala and striatum, amygdala and substantia nigra, or striatum and substantia nigra |
title | Enhanced training protects memory against amnesia produced by concurrent inactivation of amygdala and striatum, amygdala and substantia nigra, or striatum and substantia nigra |
title_full | Enhanced training protects memory against amnesia produced by concurrent inactivation of amygdala and striatum, amygdala and substantia nigra, or striatum and substantia nigra |
title_fullStr | Enhanced training protects memory against amnesia produced by concurrent inactivation of amygdala and striatum, amygdala and substantia nigra, or striatum and substantia nigra |
title_full_unstemmed | Enhanced training protects memory against amnesia produced by concurrent inactivation of amygdala and striatum, amygdala and substantia nigra, or striatum and substantia nigra |
title_short | Enhanced training protects memory against amnesia produced by concurrent inactivation of amygdala and striatum, amygdala and substantia nigra, or striatum and substantia nigra |
title_sort | enhanced training protects memory against amnesia produced by concurrent inactivation of amygdala and striatum, amygdala and substantia nigra, or striatum and substantia nigra |
topic | Neuroscience |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3243958/ https://www.ncbi.nlm.nih.gov/pubmed/22203796 http://dx.doi.org/10.3389/fnbeh.2011.00083 |
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