Neonatal sensory nerve injury-induced synaptic plasticity in the trigeminal principal sensory nucleus
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- 作者：Fu-Sun Lo ; fusunlo@gmail.com" class="auth_mail" title="E-mail the corresponding author ; Reha S. Erzurumlu
- 关键词：AMPA ; α-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid ; AHP ; after hyperpolarization ; AP ; action potential ; BSTC ; brainstem trigeminal complex ; CO ; cytochrome oxidase ; EPSP ; excitatory postsynaptic potential ; GABA ; gamma aminobutyric acid ; Iba-1 ; ionized calcium binding adaptor molecule ; ION ; infraorbital branch of the maxillary division of the trigeminal nerve ; IPSP ; inhibitory postsynaptic potential ; LTD ; long-term depression ; LTP ; long-term potentiation ; NMDA ; N-methyl-d-aspartate ; P ; pos
- 刊名：Experimental Neurology
- 出版年：2016
- 出版时间：January 2016
- 年：2016
- 卷：275
- 期：part_P2
- 页码：245-252
- 全文大小：964 K
文摘
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Neonatal sensory nerve damage alters sensory maps in the CNS and results in substantial synaptic reorganization.
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In rats and mice, neonatal infraorbital nerve lesions lead to conversion of functional synapses to silent synapses.
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Sensory nerve damage causes convergence of multipletrigeminal afferents on single neurons in the trigeminal brainstem.
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Injury-induced synaptic plasticity does not follow the timing ofthe critical period for structural plasticity.
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Effects of neonatal sensory nerve transection and crushare quite different in the CNS.