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The Functional Upregulation of Piriform Cortex Is Associated with Cross-Modal Plasticity in Loss of Whisker Tactile Inputs
BACKGROUND: Cross-modal plasticity is characterized as the hypersensitivity of remaining modalities after a sensory function is lost in rodents, which ensures their awareness to environmental changes. Cellular and molecular mechanisms underlying cross-modal sensory plasticity remain unclear. We aim...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Public Library of Science
2012
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3424151/ https://www.ncbi.nlm.nih.gov/pubmed/22927919 http://dx.doi.org/10.1371/journal.pone.0041986 |
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author | Ye, Bing Huang, Li Gao, Zilong Chen, Ping Ni, Hong Guan, Sudong Zhu, Yan Wang, Jin-Hui |
author_facet | Ye, Bing Huang, Li Gao, Zilong Chen, Ping Ni, Hong Guan, Sudong Zhu, Yan Wang, Jin-Hui |
author_sort | Ye, Bing |
collection | PubMed |
description | BACKGROUND: Cross-modal plasticity is characterized as the hypersensitivity of remaining modalities after a sensory function is lost in rodents, which ensures their awareness to environmental changes. Cellular and molecular mechanisms underlying cross-modal sensory plasticity remain unclear. We aim to study the role of different types of neurons in cross-modal plasticity. METHODOLOGY/PRINCIPAL FINDINGS: In addition to behavioral tasks in mice, whole-cell recordings at the excitatory and inhibitory neurons, and their two-photon imaging, were conducted in piriform cortex. We produced a mouse model of cross-modal sensory plasticity that olfactory function was upregulated by trimming whiskers to deprive their sensory inputs. In the meantime of olfactory hypersensitivity, pyramidal neurons and excitatory synapses were functionally upregulated, as well as GABAergic cells and inhibitory synapses were downregulated in piriform cortex from the mice of cross-modal sensory plasticity, compared with controls. A crosswire connection between barrel cortex and piriform cortex was established in cross-modal plasticity. CONCLUSION/SIGNIFICANCE: An upregulation of pyramidal neurons and a downregulation of GABAergic neurons strengthen the activities of neuronal networks in piriform cortex, which may be responsible for olfactory hypersensitivity after a loss of whisker tactile input. This finding provides the clues for developing therapeutic strategies to promote sensory recovery and substitution. |
format | Online Article Text |
id | pubmed-3424151 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2012 |
publisher | Public Library of Science |
record_format | MEDLINE/PubMed |
spelling | pubmed-34241512012-08-27 The Functional Upregulation of Piriform Cortex Is Associated with Cross-Modal Plasticity in Loss of Whisker Tactile Inputs Ye, Bing Huang, Li Gao, Zilong Chen, Ping Ni, Hong Guan, Sudong Zhu, Yan Wang, Jin-Hui PLoS One Research Article BACKGROUND: Cross-modal plasticity is characterized as the hypersensitivity of remaining modalities after a sensory function is lost in rodents, which ensures their awareness to environmental changes. Cellular and molecular mechanisms underlying cross-modal sensory plasticity remain unclear. We aim to study the role of different types of neurons in cross-modal plasticity. METHODOLOGY/PRINCIPAL FINDINGS: In addition to behavioral tasks in mice, whole-cell recordings at the excitatory and inhibitory neurons, and their two-photon imaging, were conducted in piriform cortex. We produced a mouse model of cross-modal sensory plasticity that olfactory function was upregulated by trimming whiskers to deprive their sensory inputs. In the meantime of olfactory hypersensitivity, pyramidal neurons and excitatory synapses were functionally upregulated, as well as GABAergic cells and inhibitory synapses were downregulated in piriform cortex from the mice of cross-modal sensory plasticity, compared with controls. A crosswire connection between barrel cortex and piriform cortex was established in cross-modal plasticity. CONCLUSION/SIGNIFICANCE: An upregulation of pyramidal neurons and a downregulation of GABAergic neurons strengthen the activities of neuronal networks in piriform cortex, which may be responsible for olfactory hypersensitivity after a loss of whisker tactile input. This finding provides the clues for developing therapeutic strategies to promote sensory recovery and substitution. Public Library of Science 2012-08-21 /pmc/articles/PMC3424151/ /pubmed/22927919 http://dx.doi.org/10.1371/journal.pone.0041986 Text en © 2012 Ye et al http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited. |
spellingShingle | Research Article Ye, Bing Huang, Li Gao, Zilong Chen, Ping Ni, Hong Guan, Sudong Zhu, Yan Wang, Jin-Hui The Functional Upregulation of Piriform Cortex Is Associated with Cross-Modal Plasticity in Loss of Whisker Tactile Inputs |
title | The Functional Upregulation of Piriform Cortex Is Associated with Cross-Modal Plasticity in Loss of Whisker Tactile Inputs |
title_full | The Functional Upregulation of Piriform Cortex Is Associated with Cross-Modal Plasticity in Loss of Whisker Tactile Inputs |
title_fullStr | The Functional Upregulation of Piriform Cortex Is Associated with Cross-Modal Plasticity in Loss of Whisker Tactile Inputs |
title_full_unstemmed | The Functional Upregulation of Piriform Cortex Is Associated with Cross-Modal Plasticity in Loss of Whisker Tactile Inputs |
title_short | The Functional Upregulation of Piriform Cortex Is Associated with Cross-Modal Plasticity in Loss of Whisker Tactile Inputs |
title_sort | functional upregulation of piriform cortex is associated with cross-modal plasticity in loss of whisker tactile inputs |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3424151/ https://www.ncbi.nlm.nih.gov/pubmed/22927919 http://dx.doi.org/10.1371/journal.pone.0041986 |
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