Chronic Hyperammonemia in Rats Impairs Activation of Soluble Guanylate Cyclase in Neurons and in Lymphocytes: A Putative Peripheral Marker for Neurological Alterations
- 13 April 1999
- journal article
- Published by Elsevier in Biochemical and Biophysical Research Communications
- Vol. 257 (2), 405-409
- https://doi.org/10.1006/bbrc.1999.0486
Abstract
No abstract availableKeywords
This publication has 21 references indexed in Scilit:
- Nicotine prevents glutamate-induced proteolysis of the microtubule-associated protein MAP-2 and glutamate neurotoxicity in primary cultures of cerebellar neuronsNeuropharmacology, 1998
- The beta2 subunit inhibits stimulation of the alpha1/beta1 form of soluble guanylyl cyclase by nitric oxide. Potential relevance to regulation of blood pressure.Journal of Clinical Investigation, 1997
- Ammonia Prevents Activation of NMDA Receptors by Glutamate in Rat Cerebellar Neuronal CulturesEuropean Journal of Neuroscience, 1995
- Activation of soluble guanylate cyclase through phosphorylation by protein kinase C in intact PC12 cellsBiochimica et Biophysica Acta (BBA) - Molecular Cell Research, 1993
- Glutamatergic synaptic dysfunction in hyperammonemic syndromesMetabolic Brain Disease, 1992
- Opposite effects of arachidonic acid and of its hydroperoxides on brain soluble guanylate cyclase activityNeurochemistry International, 1991
- A simple animal model of hyperammonemiaHepatology, 1989
- Activation of soluble guanylate cyclase by arachidonic acid and 15-lipoxygenase productsBiochimica et Biophysica Acta (BBA) - Molecular Cell Research, 1986
- The Release and Neosynthesis of Glutamic Acid Are Increased in Experimental Models of Hepatic EncephalopathyJournal of Neurochemistry, 1983
- Evidence for phosphorylation of rat brain guanylate cyclase by cyclic AMP-dependent protein kinaseBiochemical and Biophysical Research Communications, 1981