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Titolo:
Glutamate transporter and receptor function in disorders of ammonia metabolism
Autore:
Butterworth, RF;
Indirizzi:
Univ Montreal, CHUM, Hop St Luc, Neurosci Res Unit, Montreal, PQ H2X 3J4, Canada Univ Montreal Montreal PQ Canada H2X 3J4 it, Montreal, PQ H2X 3J4, Canada
Titolo Testata:
MENTAL RETARDATION AND DEVELOPMENTAL DISABILITIES RESEARCH REVIEWS
fascicolo: 4, volume: 7, anno: 2001,
pagine: 276 - 279
SICI:
1080-4013(2001)7:4<276:GTARFI>2.0.ZU;2-C
Fonte:
ISI
Lingua:
ENG
Soggetto:
ACUTE LIVER-FAILURE; HEPATIC-ENCEPHALOPATHY; RAT-BRAIN; ENERGY-METABOLISM; FRONTAL-CORTEX; SELECTIVE LOSS; BINDING-SITES; AMINO-ACIDS; ASPARTATE; HYPERAMMONEMIA;
Keywords:
glutamate; ammonia; hyperammonemia; urea cycle disorders; liver failure; glutamate transporters; GLT-1; GLAST; NMDA receptors;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
25
Recensione:
Indirizzi per estratti:
Indirizzo: Butterworth, RF Univ Montreal, CHUM, Hop St Luc, Neurosci Res Unit, 1058 St Denis St, Montreal, PQ H2X 3J4, Canada Univ Montreal 1058 St Denis St Montreal PQ Canada H2X 3J4
Citazione:
R.F. Butterworth, "Glutamate transporter and receptor function in disorders of ammonia metabolism", MENT RET D, 7(4), 2001, pp. 276-279

Abstract

Disorders of ammonia metabolism including urea cycle enzymopathies, Reye Syndrome, and liver failure are associated with brain edema and severe neurological impairment. Excess blood-borne ammonia crosses the blood-brain barrier by diffusion as NH3 where it interacts with various cellular processes involved in neurotransmission and brain energy metabolism. Ammonia exerts apotent effect on glutamate (AMPA) receptor-mediated neurotransmission. Ammonia also inhibits high affinity transport of glutamate by an action on astrocytic glutamate transporter expression, an action which results in increased extracellular concentrations of glutamate. Acute hyperammonemia directly activates the NMDA subclass of glutamate receptors resulting in increasedintracellular Ca2+ and increased synthesis of nitric oxide and cGMP. Chronic hyperammonemia, on the other hand, results in a loss of NMDA receptor sites. Activation of NMDA receptors in acute ammonia toxicity results in depletion of ATP in brain. Neuropathologic studies in experimental animals withcongenital urea cycle disorders and severe hyperammonemia reveal evidence of neuronal cell death which is excitotoxic in nature. These findings suggest that overactivation of NMDA receptors is a significant feature of acute hyperammonemic syndromes and that antagonists of these receptors or of their signal transduction pathway enzymes such as nNOS could be beneficial in the treatment of the central nervous system manifestations (encephalopathy, brain edema) which are characteristic of hyperammonemic disorders. (C) 2001Wiley-Liss, Inc.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 28/01/20 alle ore 14:42:35