Brain research · 2014
Transient down-regulation and restoration of glycogen synthase levels in axotomized rat facial motoneurons.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Takezawa Yosuke, Kohsaka Shinichi, Nakajima Kazuyuki
Аннотация
In adult rats, transection of the facial nerve causes a functional down-regulation of motoneurons and glial activation/proliferation. It has not been clear how energy-supplying systems are regulated in an axotomized facial nucleus. Here we investigated the regulation of molecules involved in glycogen degradation/synthesis in axotomized facial nuclei in rats. Immunoblotting revealed that the amounts of glycogen phosphorylase in the contralateral and ipsilateral nuclei were unchanged for the first 14 days, whereas the amount of glycogen synthase in the axotomized facial nuclei was significantly decreased from days 7-14 post-insult. A quantitative analysis estimated that the glycogen synthase levels in the transected nucleus were reduced to approx. 50% at 14 days post-injury. An immunohistochemical study showed that the injured motoneurons had decreased expressions of glycogen synthase proteins. The glycogen synthase levels in the axotomized facial nucleus had returned to control levels by 5 weeks post-insult, as had the cholinergic markers. The immunohistochemical study also revealed the recovery of glycogen synthase levels at the later stage. The glycogen phosphorylase levels in the injured nucleus were not significantly changed during weeks 3-5 post-insult. Taken together, these results demonstrated that the injured facial motoneurons transiently reduced glycogen synthase levels at around 1-2 weeks post-insult, but restored the levels at 4-5 weeks post-insult.
Предметные рубрики MeSH
AnimalsAxotomyCD11b AntigenCalcium-Binding ProteinsCell CountDown-RegulationFacial Nerve InjuriesFunctional LateralityGlial Fibrillary Acidic ProteinGlycogen PhosphorylaseGlycogen SynthaseMaleMicrofilament ProteinsMotor NeuronsRatsRats, WistarReceptors, N-Methyl-D-AspartateRecovery of FunctionTime FactorsVesicular Acetylcholine Transport Proteins