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Molecular Mechanisms Involved in Depotentiation and Their Relevance to Schizophrenia
Long-term potentiation (LTP) and long-term depression (LTD) of synaptic transmission are forms of synaptic plasticity that have been studied extensively and are thought to contribute to learning and memory. The reversal of LTP, known as depotentiation (DP) has received far less attention however, an...
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Chonnam National University Medical School
2012
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3341431/ https://www.ncbi.nlm.nih.gov/pubmed/22570808 http://dx.doi.org/10.4068/cmj.2012.48.1.1 |
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author | Sanderson, Thomas M |
author_facet | Sanderson, Thomas M |
author_sort | Sanderson, Thomas M |
collection | PubMed |
description | Long-term potentiation (LTP) and long-term depression (LTD) of synaptic transmission are forms of synaptic plasticity that have been studied extensively and are thought to contribute to learning and memory. The reversal of LTP, known as depotentiation (DP) has received far less attention however, and its role in behavior is also far from clear. Recently, deficits in depotentiation have been observed in models of schizophrenia, suggesting that a greater understanding of this form of synaptic plasticity may help reveal the physiological alterations that underlie symptoms experienced by patients. This review therefore seeks to summarize the current state of knowledge on DP, and then put the deficits in DP in models of disease into this context. |
format | Online Article Text |
id | pubmed-3341431 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2012 |
publisher | Chonnam National University Medical School |
record_format | MEDLINE/PubMed |
spelling | pubmed-33414312012-05-08 Molecular Mechanisms Involved in Depotentiation and Their Relevance to Schizophrenia Sanderson, Thomas M Chonnam Med J Review Article Long-term potentiation (LTP) and long-term depression (LTD) of synaptic transmission are forms of synaptic plasticity that have been studied extensively and are thought to contribute to learning and memory. The reversal of LTP, known as depotentiation (DP) has received far less attention however, and its role in behavior is also far from clear. Recently, deficits in depotentiation have been observed in models of schizophrenia, suggesting that a greater understanding of this form of synaptic plasticity may help reveal the physiological alterations that underlie symptoms experienced by patients. This review therefore seeks to summarize the current state of knowledge on DP, and then put the deficits in DP in models of disease into this context. Chonnam National University Medical School 2012-04 2012-04-26 /pmc/articles/PMC3341431/ /pubmed/22570808 http://dx.doi.org/10.4068/cmj.2012.48.1.1 Text en © Chonnam Medical Journal, 2012 http://creativecommons.org/licenses/by-nc/3.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Review Article Sanderson, Thomas M Molecular Mechanisms Involved in Depotentiation and Their Relevance to Schizophrenia |
title | Molecular Mechanisms Involved in Depotentiation and Their Relevance to Schizophrenia |
title_full | Molecular Mechanisms Involved in Depotentiation and Their Relevance to Schizophrenia |
title_fullStr | Molecular Mechanisms Involved in Depotentiation and Their Relevance to Schizophrenia |
title_full_unstemmed | Molecular Mechanisms Involved in Depotentiation and Their Relevance to Schizophrenia |
title_short | Molecular Mechanisms Involved in Depotentiation and Their Relevance to Schizophrenia |
title_sort | molecular mechanisms involved in depotentiation and their relevance to schizophrenia |
topic | Review Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3341431/ https://www.ncbi.nlm.nih.gov/pubmed/22570808 http://dx.doi.org/10.4068/cmj.2012.48.1.1 |
work_keys_str_mv | AT sandersonthomasm molecularmechanismsinvolvedindepotentiationandtheirrelevancetoschizophrenia |