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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Summary: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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ISSN:1756-6606
1756-6606
DOI:10.1186/1756-6606-6-2