Upregulation of excitatory neurons and downregulation of inhibitory neurons in barrel cortex are associated with loss of whisker inputs
Loss of a sensory input causes the hypersensitivity in other modalities. In addition to cross-modal plasticity, the sensory cortices without receiving inputs undergo the plastic changes. It is not clear how the different types of neurons and synapses in the sensory cortex coordinately change after i...
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Published in | Molecular brain Vol. 6; no. 1; p. 2 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
London
BioMed Central
03.01.2013
BioMed Central Ltd BMC |
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Online Access | Get full text |
ISSN | 1756-6606 1756-6606 |
DOI | 10.1186/1756-6606-6-2 |
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Abstract | Loss of a sensory input causes the hypersensitivity in other modalities. In addition to cross-modal plasticity, the sensory cortices without receiving inputs undergo the plastic changes. It is not clear how the different types of neurons and synapses in the sensory cortex coordinately change after input deficits in order to prevent loss of their functions and to be used for other modalities. We studied this subject in the barrel cortices from whiskers-trimmed mice vs. controls. After whisker trimming for a week, the intrinsic properties of pyramidal neurons and the transmission of excitatory synapses were upregulated in the barrel cortex, but inhibitory neurons and GABAergic synapses were downregulated. The morphological analyses indicated that the number of processes and spines in pyramidal neurons increased, whereas the processes of GABAergic neurons decreased in the barrel cortex. The upregulation of excitatory neurons and the downregulation of inhibitory neurons boost the activity of network neurons in the barrel cortex to be high levels, which prevent the loss of their functions and enhances their sensitivity to sensory inputs. These changes may prepare for attracting the innervations from sensory cortices and/or peripheral nerves for other modalities during cross-modal plasticity. |
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AbstractList | Loss of a sensory input causes the hypersensitivity in other modalities. In addition to cross-modal plasticity, the sensory cortices without receiving inputs undergo the plastic changes. It is not clear how the different types of neurons and synapses in the sensory cortex coordinately change after input deficits in order to prevent loss of their functions and to be used for other modalities. We studied this subject in the barrel cortices from whiskers-trimmed mice vs. controls. After whisker trimming for a week, the intrinsic properties of pyramidal neurons and the transmission of excitatory synapses were upregulated in the barrel cortex, but inhibitory neurons and GABAergic synapses were downregulated. The morphological analyses indicated that the number of processes and spines in pyramidal neurons increased, whereas the processes of GABAergic neurons decreased in the barrel cortex. The upregulation of excitatory neurons and the downregulation of inhibitory neurons boost the activity of network neurons in the barrel cortex to be high levels, which prevent the loss of their functions and enhances their sensitivity to sensory inputs. These changes may prepare for attracting the innervations from sensory cortices and/or peripheral nerves for other modalities during cross-modal plasticity. Loss of a sensory input causes the hypersensitivity in other modalities. In addition to cross-modal plasticity, the sensory cortices without receiving inputs undergo the plastic changes. It is not clear how the different types of neurons and synapses in the sensory cortex coordinately change after input deficits in order to prevent loss of their functions and to be used for other modalities. We studied this subject in the barrel cortices from whiskers-trimmed mice vs. controls. After whisker trimming for a week, the intrinsic properties of pyramidal neurons and the transmission of excitatory synapses were upregulated in the barrel cortex, but inhibitory neurons and GABAergic synapses were downregulated. The morphological analyses indicated that the number of processes and spines in pyramidal neurons increased, whereas the processes of GABAergic neurons decreased in the barrel cortex. The upregulation of excitatory neurons and the downregulation of inhibitory neurons boost the activity of network neurons in the barrel cortex to be high levels, which prevent the loss of their functions and enhances their sensitivity to sensory inputs. These changes may prepare for attracting the innervations from sensory cortices and/or peripheral nerves for other modalities during cross-modal plasticity. Keywords: Neural plasticity, Neuron, Synapse, GABA, Glutamate, Barrel cortex and whisker Loss of a sensory input causes the hypersensitivity in other modalities. In addition to cross-modal plasticity, the sensory cortices without receiving inputs undergo the plastic changes. It is not clear how the different types of neurons and synapses in the sensory cortex coordinately change after input deficits in order to prevent loss of their functions and to be used for other modalities. We studied this subject in the barrel cortices from whiskers-trimmed mice vs. controls. After whisker trimming for a week, the intrinsic properties of pyramidal neurons and the transmission of excitatory synapses were upregulated in the barrel cortex, but inhibitory neurons and GABAergic synapses were downregulated. The morphological analyses indicated that the number of processes and spines in pyramidal neurons increased, whereas the processes of GABAergic neurons decreased in the barrel cortex. The upregulation of excitatory neurons and the downregulation of inhibitory neurons boost the activity of network neurons in the barrel cortex to be high levels, which prevent the loss of their functions and enhances their sensitivity to sensory inputs. These changes may prepare for attracting the innervations from sensory cortices and/or peripheral nerves for other modalities during cross-modal plasticity.Loss of a sensory input causes the hypersensitivity in other modalities. In addition to cross-modal plasticity, the sensory cortices without receiving inputs undergo the plastic changes. It is not clear how the different types of neurons and synapses in the sensory cortex coordinately change after input deficits in order to prevent loss of their functions and to be used for other modalities. We studied this subject in the barrel cortices from whiskers-trimmed mice vs. controls. After whisker trimming for a week, the intrinsic properties of pyramidal neurons and the transmission of excitatory synapses were upregulated in the barrel cortex, but inhibitory neurons and GABAergic synapses were downregulated. The morphological analyses indicated that the number of processes and spines in pyramidal neurons increased, whereas the processes of GABAergic neurons decreased in the barrel cortex. The upregulation of excitatory neurons and the downregulation of inhibitory neurons boost the activity of network neurons in the barrel cortex to be high levels, which prevent the loss of their functions and enhances their sensitivity to sensory inputs. These changes may prepare for attracting the innervations from sensory cortices and/or peripheral nerves for other modalities during cross-modal plasticity. Doc number: 2 Abstract: Loss of a sensory input causes the hypersensitivity in other modalities. In addition to cross-modal plasticity, the sensory cortices without receiving inputs undergo the plastic changes. It is not clear how the different types of neurons and synapses in the sensory cortex coordinately change after input deficits in order to prevent loss of their functions and to be used for other modalities. We studied this subject in the barrel cortices from whiskers-trimmed mice vs. controls. After whisker trimming for a week, the intrinsic properties of pyramidal neurons and the transmission of excitatory synapses were upregulated in the barrel cortex, but inhibitory neurons and GABAergic synapses were downregulated. The morphological analyses indicated that the number of processes and spines in pyramidal neurons increased, whereas the processes of GABAergic neurons decreased in the barrel cortex. The upregulation of excitatory neurons and the downregulation of inhibitory neurons boost the activity of network neurons in the barrel cortex to be high levels, which prevent the loss of their functions and enhances their sensitivity to sensory inputs. These changes may prepare for attracting the innervations from sensory cortices and/or peripheral nerves for other modalities during cross-modal plasticity. Abstract Loss of a sensory input causes the hypersensitivity in other modalities. In addition to cross-modal plasticity, the sensory cortices without receiving inputs undergo the plastic changes. It is not clear how the different types of neurons and synapses in the sensory cortex coordinately change after input deficits in order to prevent loss of their functions and to be used for other modalities. We studied this subject in the barrel cortices from whiskers-trimmed mice vs. controls. After whisker trimming for a week, the intrinsic properties of pyramidal neurons and the transmission of excitatory synapses were upregulated in the barrel cortex, but inhibitory neurons and GABAergic synapses were downregulated. The morphological analyses indicated that the number of processes and spines in pyramidal neurons increased, whereas the processes of GABAergic neurons decreased in the barrel cortex. The upregulation of excitatory neurons and the downregulation of inhibitory neurons boost the activity of network neurons in the barrel cortex to be high levels, which prevent the loss of their functions and enhances their sensitivity to sensory inputs. These changes may prepare for attracting the innervations from sensory cortices and/or peripheral nerves for other modalities during cross-modal plasticity. |
ArticleNumber | 2 |
Audience | Academic |
Author | Zhang, Guanjun Wang, Jin-Hui Gao, Zilong Guan, Sudong Zhu, Yan |
AuthorAffiliation | 2 State Key Lab of Brain and Cognitive Science, Institute of Biophysics, Chinese Academy of Sciences, Beijing 100101, China 1 Department of Physiology, Bengbu Medical College, Bengbu, Anhui Province 233000, China 3 University of Chinese Academy of Sciences, Beijing 100049, China |
AuthorAffiliation_xml | – name: 2 State Key Lab of Brain and Cognitive Science, Institute of Biophysics, Chinese Academy of Sciences, Beijing 100101, China – name: 1 Department of Physiology, Bengbu Medical College, Bengbu, Anhui Province 233000, China – name: 3 University of Chinese Academy of Sciences, Beijing 100049, China |
Author_xml | – sequence: 1 givenname: Guanjun surname: Zhang fullname: Zhang, Guanjun organization: Department of Physiology, Bengbu Medical College – sequence: 2 givenname: Zilong surname: Gao fullname: Gao, Zilong organization: State Key Lab of Brain and Cognitive Science, Institute of Biophysics, Chinese Academy of Sciences, University of Chinese Academy of Sciences – sequence: 3 givenname: Sudong surname: Guan fullname: Guan, Sudong organization: Department of Physiology, Bengbu Medical College – sequence: 4 givenname: Yan surname: Zhu fullname: Zhu, Yan organization: Department of Physiology, Bengbu Medical College – sequence: 5 givenname: Jin-Hui surname: Wang fullname: Wang, Jin-Hui email: jhw@sun5.ibp.ac.cn organization: Department of Physiology, Bengbu Medical College, State Key Lab of Brain and Cognitive Science, Institute of Biophysics, Chinese Academy of Sciences, University of Chinese Academy of Sciences |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/23286328$$D View this record in MEDLINE/PubMed |
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Copyright | Zhang et al.; licensee BioMed Central Ltd. 2013 This article is published under license to BioMed Central Ltd. 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 work is properly cited. COPYRIGHT 2013 BioMed Central Ltd. 2013 Zhang et al.; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Copyright ©2013 Zhang et al.; licensee BioMed Central Ltd. 2013 Zhang et al.; licensee BioMed Central Ltd. |
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Keywords | Barrel cortex and whisker GABA Neural plasticity Synapse Neuron Glutamate |
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Snippet | Loss of a sensory input causes the hypersensitivity in other modalities. In addition to cross-modal plasticity, the sensory cortices without receiving inputs... Doc number: 2 Abstract: Loss of a sensory input causes the hypersensitivity in other modalities. In addition to cross-modal plasticity, the sensory cortices... Abstract Loss of a sensory input causes the hypersensitivity in other modalities. In addition to cross-modal plasticity, the sensory cortices without receiving... |
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SubjectTerms | Action Potentials - physiology Analysis Animals Barrel cortex and whisker Biomedical and Life Sciences Biomedicine Brain Cortex (barrel) Cortex (somatosensory) Cross-modal Dendrites - physiology Dendritic spines Down-Regulation GABA GABAergic Neurons - metabolism gamma -Aminobutyric acid Glutamate Hypersensitivity Innervation Mice Mice, Inbred C57BL Neural Inhibition - physiology Neural plasticity Neurology Neuron Neurons Neurons - physiology Neurophysiology Neurosciences Neurotransmission Peripheral nerves Plasticity Proteins Psychopharmacology Pyramidal cells Pyramidal Cells - metabolism Sensory evaluation Somatosensory Cortex - physiology Synapse Synapses Synapses - metabolism Up-Regulation Vibrissae - innervation Vibrissae - metabolism |
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Title | Upregulation of excitatory neurons and downregulation of inhibitory neurons in barrel cortex are associated with loss of whisker inputs |
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