Gene expression of NMDA and AMPA receptors in different facial motor neurons

Chen, Pei; Song, Jun; Luo, Lan; Cheng, Qing; Xiao, Hongjun; Gong, Shusheng

doi:10.1002/lary.25575

Cited by 4 publications

(1 citation statement)

References 31 publications

(92 reference statements)

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“…Motoneurons actually express both excitatory glutamate (Glu) receptors and inhibitory gamma-amino butyric acid (GABA) receptors on their surfaces, and the levels of both receptor types were found to be affected by facial nerve transection, similar to the cases of ChAT and VAChT. Ionotropic glutamate receptors (GluRs) including N-methyl-D-aspartate (NMDA) receptors (NR1 and NR2A/2B) and alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptors were detected in facial motoneurons [37,38]. On the cell membrane, these receptors respond to any excitatory drive including the commands sent from upper motoneurons in the cortex.…”

Section: Function-related Moleculesmentioning

confidence: 87%

Events Occurring in the Axotomized Facial Nucleus

Nakajima

Ishijima

2022

Cells

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Transection of the rat facial nerve leads to a variety of alterations not only in motoneurons, but also in glial cells and inhibitory neurons in the ipsilateral facial nucleus. In injured motoneurons, the levels of energy metabolism-related molecules are elevated, while those of neurofunction-related molecules are decreased. In tandem with these motoneuron changes, microglia are activated and start to proliferate around injured motoneurons, and astrocytes become activated for a long period without mitosis. Inhibitory GABAergic neurons reduce the levels of neurofunction-related molecules. These facts indicate that injured motoneurons somehow closely interact with glial cells and inhibitory neurons. At the same time, these events allow us to predict the occurrence of tissue remodeling in the axotomized facial nucleus. This review summarizes the events occurring in the axotomized facial nucleus and the cellular and molecular mechanisms associated with each event.

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Section: Function-related Moleculesmentioning

confidence: 87%

Events Occurring in the Axotomized Facial Nucleus

Nakajima

Ishijima

2022

Cells

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Response of the GABAergic System to Axotomy of the Rat Facial Nerve

et al. 2017

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The responses of inhibitory neurons/synapses to motoneuron injury in the cranial nervous system remain to be elucidated. In this study, we analyzed GABA receptor (GABAR) and GABAergic neurons at the protein level in the transected rat facial nucleus. Immunoblotting revealed that the GABARα1 protein levels in the axotomized facial nucleus decreased significantly 5-14 days post-insult, and these levels remained low for 5 weeks. Immunohistochemical analysis indicated that the GABARα1-expressing cells were motoneurons. We next examined the specific components of GABAergic neurons, including glutamate decarboxylase (GAD), vesicular GABA transporter (VGAT) and GABA transporter-1 (GAT-1). Immunoblotting indicated that the protein levels of GAD, VGAT and GAT-1 decreased transiently in the transected facial nucleus from 5 to 14 days post-insult, but returned to the control levels at 5 weeks post-insult. Although GABARα1 protein levels in the transected nucleus did not return to their control levels for 5 weeks post-insult, the administration of glial cell line-derived neurotrophic factor at the cut site significantly ameliorated the reductions. Through these findings, we verified that the injured facial motoneurons suppressed the levels of GABARα1 protein over the 5 weeks post-insult, presumably due to the deprivation of neurotrophic factor. On the other hand, the levels of the GAD, VGAT and GAT-1 proteins in GABAergic neurons were transiently reduced in the axotomized facial nucleus at 5-14 days post-insult, but recovered at 4-5 weeks post-insult.

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IGF-1-Involved Negative Feedback of NR2B NMDA Subunits Protects Cultured Hippocampal Neurons Against NMDA-Induced Excitotoxicity

Sun

Han

et al. 2016

Mol Neurobiol

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Insulin-like growth factor 1 (IGF-1) is a multifunctional protein involved in neuronal polarity and axonal guidance. In our previous study, it was discovered that IGF-1 alleviated 50-μM NMDA-induced excitotoxicity against neuronal autophagy via depression of NR2B p-Ser1303 activation. However, it was found that NMDA at a higher dose did not cause neuronal autophagy. And, the performance of IGF-1 under severe excitotoxicity still needs to be clarified. In this study, we observed that IGF-1 can salvage the hippocampal neurons in an autophagy-independent manner after 150-μM NMDA exposure using thiazolyl blue tetrazolium bromide (MTT), lactate dehydrogenase (LDH), Western blot assay, and transmission electron microscopy. In addition, over-activation of post-synaptic NMDARs was found with the whole-cell patch clamp recording method. In order to explore whether there is a positive feedback way for post-synaptic NMDARs and the different pathway caused by 150 μM NMDA, the phosphorylation level of Fyn and the phosphorylation site of NR2B were investigated. It was observed that NR2B p-Tyr1472 was increased by the activation of Fyn after 150-μM NMDA exposure. When the neutralizing antibody against NR2B p-Ser1303 was added into the medium, both the activations of Fyn and NR2B p-Tyr1472 were blocked, suggesting NR2B p-Ser1303 may be the initial step of NMDA-induced excitotoxicity. In addition, since IGF-1 can block the initial step of NR2B activation, its effect is concluded to continue with the development of excitotoxicity. Overall, this study strongly indicates that the relationship between different phosphorylation sites of NR2B should be laid more emphasis on, which may be a vital target for the NR2B-involved excitotoxicity.

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Gene expression of NMDA and AMPA receptors in different facial motor neurons

Cited by 4 publications

References 31 publications

Events Occurring in the Axotomized Facial Nucleus

Events Occurring in the Axotomized Facial Nucleus

Response of the GABAergic System to Axotomy of the Rat Facial Nerve

IGF-1-Involved Negative Feedback of NR2B NMDA Subunits Protects Cultured Hippocampal Neurons Against NMDA-Induced Excitotoxicity

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