Current neurobiology最新文献

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IFNγ Increases M2 Muscarinic Receptor Expression in Cultured Sympathetic Neurons. IFNγ增加培养交感神经元M2毒蕈碱受体的表达。

Current neurobiology Pub Date : 2011-04-01

Ana Cristina G Grodzki, Atefeh Ghogha, Linley Mangini, Allison D Fryer, Pamela J Lein

{"title":"IFNγ Increases M2 Muscarinic Receptor Expression in Cultured Sympathetic Neurons.","authors":"Ana Cristina G Grodzki, Atefeh Ghogha, Linley Mangini, Allison D Fryer, Pamela J Lein","doi":"","DOIUrl":"","url":null,"abstract":"M2 muscarinic receptors are expressed on both parasympathetic and sympathetic nerve endings where they function as autoinhibitory receptors to limit release of acetylcholine and norepinephrine, respectively. M2 muscarinic receptor expression on parasympathetic nerves is decreased by viral infection and by gamma-interferon (IFNγ) and increased by dexamethasone; and these effects are of clinical relevance in the etiology and treatment of asthma. Whether IFNγ and dexamethasone similarly modulate M2 receptor expression on sympathetic nerves is not known. To address this question, we examined the effects of IFNγ and dexamethasone on M2 receptor expression at the mRNA and protein level in primary cultures of sympathetic neurons dissociated from the rat superior cervical ganglia (SCG). Semi-quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) indicated that neither IFNγ nor dexamethasone altered M2 receptor transcript levels. However, western blot analyses demonstrated that IFNγ, but not dexamethasone, increases M2 receptor protein expression in sympathetic neurons. Increased expression did not significantly alter subcellular localization of M2 receptors in sympathetic neurons as determined using immunocytochemistry. These findings indicate that M2 receptors are differentially regulated in different types of autonomic neurons, and they suggest a novel mechanism by which IFNγ may contribute to airway hyperreactivity in viral-induced asthma.","PeriodicalId":89670,"journal":{"name":"Current neurobiology","volume":"2 1","pages":"23-29"},"PeriodicalIF":0.0,"publicationDate":"2011-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3515643/pdf/nihms419211.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31111411","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Method for Shipping Live Cultures of Dissociated Rat Hippocampal Neurons. 游离大鼠海马神经元活体培养物的运输方法。

Current neurobiology Pub Date : 2010-10-01

Dongren Yang, Donald Bruun, Douglas A Andres, Pamela J Lein

引用次数: 0

Polychlorinated biphenyls increase apoptosis in the developing rat brain. 多氯联苯增加发育中的大鼠脑细胞凋亡。

Current neurobiology Pub Date : 2010-03-01

Dongren Yang, Pamela J Lein

{"title":"Polychlorinated biphenyls increase apoptosis in the developing rat brain.","authors":"Dongren Yang, Pamela J Lein","doi":"","DOIUrl":"","url":null,"abstract":"While both epidemiological and experimental animal studies have demonstrated that perinatal exposure to polychlorinated biphenyls (PCBs) negatively impacts cognitive and psychomotor function, there remains considerable uncertainty regarding mechanisms by which PCBs cause these functional deficits. In vitro studies have shown that PCBs can trigger apoptosis in cultured neurons and suggest this effect is mediated in part by increased levels of reactive oxygen species (ROS). However, whether PCBs cause similar effects in vivo in the developing brain has yet to be reported. In this study, rat pups were exposed to the commercial PCB mixture Aroclor 1254 (A1254) at 0.1 or 1.0 mg/kg/d in the maternal diet throughout gestation and lactation. Apoptosis and oxidative damage were quantified in three brain regions within several days after birth and at weaning. Caspase-3 activity was significantly increased in the cortex, hippocampus and cerebellum of newborn but not weanling rats exposed to A1254 at 1.0 mg/kg/d in the maternal diet. The most prominent effect was observed in the cerebellum, and PCB-induced apoptosis in this brain region was confirmed by TUNEL. Western blotting revealed that developmental A1254 exposure also increased levels of 3-nitrotyrosine and 4-hydroxynonenal levels in the cerebellum of new-born rats, indicating increased oxidative damage of proteins and lipids, respectively. These findings provide the first in vivo data in support of the hypothesis that PCB-induced oxidative stress alters spatiotemporal profiles of apoptosis, and suggest that this is an important mechanism contributing to the developmental neurotoxicity of PCBs.","PeriodicalId":89670,"journal":{"name":"Current neurobiology","volume":"1 1","pages":"70-76"},"PeriodicalIF":0.0,"publicationDate":"2010-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3775291/pdf/nihms-417981.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31747365","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

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