Research article summary (published 21 Dec 2008):

Identifying the direct effects of ammonia on the brain.

Full Abstract

Elevated concentrations of ammonia in the brain as a result of hyperammonemia leads to cerebral dysfunction involving a spectrum of neuropsychiatric and neurological symptoms (impaired memory, shortened attention span, sleep-wake inversions, brain edema, intracranial hypertension, seizures, ataxia and coma). Many studies have demonstrated ammonia as a major player involved in the neuropathophysiology associated with liver failure and inherited urea cycle enzyme disorders. Ammonia in solution is composed of a gas (NH(3)) and an ionic (NH(4) (+)) component which are both capable of crossing plasma membranes through diffusion, channels and transport mechanisms and as a result have a direct effect on pH. Furthermore, NH(4) (+) has similar properties as K(+) and, therefore, competes with K(+) on K(+) transporters and channels resulting in a direct effect on membrane potential. Ammonia is also a product as well as a substrate for many different biochemical reactions and consequently, an increase in brain ammonia accompanies disturbances in cerebral metabolism. These direct effects of elevated ammonia concentrations on the brain will lead to a cascade of secondary effects and encephalopathy.

Author information

Author/s: Bosoi, Cristina R (CR); Rose, Christopher F (CF);

Affiliation: Neuroscience Research Unit, Hôpital Saint-Luc (CRCHUM), Université de Montreal, 264, boulevard René Lévesque Est, H2X 1P1, Montréal, Québec, Canada.

Journal and publication information

Publication Type: Journal Article; Review

Journal: Metabolic brain disease (Metab Brain Dis), published in United States. (Language: eng)

Reference: 2009-Mar; vol 24 (issue 1) : pp 95-102

Dates: Created 2009/02/13; Completed 2009/07/06;

PMID: 19104924, status: MEDLINE (last retrieved date: 7/24/2009)

Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.

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MeSH headings (categories)

This article was linked to the MeSH Headings (categories) shown below.

Adenosine Triphosphatases - metabolism Ammonia - metabolism Animals Brain - metabolism; physiopathology Cation Transport Proteins - metabolism Cell Membrane - metabolism

Cell Membrane - metabolism Hepatic Encephalopathy - metabolism; physiopathology Humans Hyperammonemia - metabolism; physiopathology Membrane Potential, Mitochondrial - physiology Neurons - metabolism

Note: Bold headings indicate primary MeSH headings or qualifiers.

Associated Chemicals: Cation Transport Proteins (0) ; Ammonia (7664-41-7) ; Adenosine Triphosphatases (EC 3.6.1.-) ; potassium transporting ATPase (EC 3.6.1.-)

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