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Chronic hyperammonemia alters protein phosphorylation and glutamate receptor-associated signal transduction in brain.

Abstract：

:There is substantial evidence that hyperammonemia is one of the main factors contributing to the neurological alterations found in hepatic encephalopathy. The mechanisms by which chronic moderate hyperammonemia affects brain function involves alterations in neurotransmission at different steps. This article reviews the effects of hyperammonemia on phosphorylation of key brain proteins involved in neurotransmission (the microtubule-associated protein (MAP-2), Na+/K+-ATPase and NMDA receptors). The physiological function of these proteins is modulated by phosphorylation and its altered phosphorylation in hyperammonemia may contribute to impairment of neurotransmission. The effects of chronic hyperammonemia on signal transduction pathways associated to glutamate receptors, such as the glutamate-nitric oxide (NO)-cGMP pathway, are also reviewed. The possible contribution of the impairment of this pathway in brain in vivo to the neurological alterations present in patients with hepatic encephalopathy is discussed.

journal_name

Neurochem Int

journal_title

Neurochemistry international

authors

Corbalán R,Hernández-Viadel M,Llansola M,Montoliu C,Felipo V

doi

10.1016/s0197-0186(02)00030-x

subject

Has Abstract

pub_date

2002-08-01 00:00:00

pages

103-8

issue

2-3

eissn

0197-0186

issn

1872-9754

pii

S019701860200030X

journal_volume

41

pub_type

杂志文章,评审

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