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 inMolecular brain Vol. 6; no. 1; p. 2
Main Authors Zhang, Guanjun, Gao, Zilong, Guan, Sudong, Zhu, Yan, Wang, Jin-Hui
Format Journal Article
LanguageEnglish
Published London BioMed Central 03.01.2013
BioMed Central Ltd
BMC
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ISSN1756-6606
1756-6606
DOI10.1186/1756-6606-6-2

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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.
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
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– name: 1 Department of Physiology, Bengbu Medical College, Bengbu, Anhui Province 233000, China
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Keywords Barrel cortex and whisker
GABA
Neural plasticity
Synapse
Neuron
Glutamate
Language English
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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
URI https://link.springer.com/article/10.1186/1756-6606-6-2
https://www.ncbi.nlm.nih.gov/pubmed/23286328
https://www.proquest.com/docview/1270643032
https://www.proquest.com/docview/1273702450
https://www.proquest.com/docview/1285096544
http://dx.doi.org/10.1186/1756-6606-6-2
https://pubmed.ncbi.nlm.nih.gov/PMC3548736
https://doaj.org/article/850e1d1977704b0496691f25b613bd3d
Volume 6
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