کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9989721 | 1580764 | 2005 | 12 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Neurons exposed to ammonia reproduce the differential alteration in nitric oxide modulation of guanylate cyclase in the cerebellum and cortex of patients with liver cirrhosis
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
عصب شناسی
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چکیده انگلیسی
The activation of soluble guanylate cyclase by nitric oxide is increased in the frontal cortex but is reduced in the cerebellum of patients who died with liver cirrhosis. The aims of this work were to assess whether hyperammonemia is responsible for the region-selective alterations in guanylate cyclase modulation in liver cirrhosis and to assess whether the alteration occurs in neurons or in astrocytes. The activation of guanylate cyclase by nitric oxide was lower in cerebellar neurons exposed to ammonia (1.5-fold) than in control neurons (3.3-fold). The activation of guanylate cyclase by nitric oxide was higher in cortical neurons exposed to ammonia (8.7-fold) than in control neurons (5.5-fold). The activation was not affected in cerebellar or cortical astrocytes. These findings indicate that hyperammonemia is responsible for the differential alterations in the modulation of soluble guanylate cyclase in cerebellum and cerebral cortex of cirrhotic patients. Moreover, the alterations occur specifically in neurons and not in astrocytes.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neurobiology of Disease - Volume 19, Issues 1â2, JuneâJuly 2005, Pages 150-161
Journal: Neurobiology of Disease - Volume 19, Issues 1â2, JuneâJuly 2005, Pages 150-161
نویسندگان
Regina Rodrigo, Slaven Erceg, Vicente Felipo,