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Titolo:
Hyperammonemia impairs NMDA receptor-dependent long-term potentiation in the CA1 of rat hippocampus in vitro
Autore:
Munoz, MD; Monfort, P; Gaztelu, JM; Felipo, V;
Indirizzi:
Hosp Ramon y Cajal, Dept Invest, CSIC, E-28034 Madrid, Spain Hosp Ramon y Cajal Madrid Spain E-28034 est, CSIC, E-28034 Madrid, Spain Fdn Valenciana Invest Biomed, Inst Invest Citol, Valencia 46010, Spain FdnValenciana Invest Biomed Valencia Spain 46010 Valencia 46010, Spain
Titolo Testata:
NEUROCHEMICAL RESEARCH
fascicolo: 4, volume: 25, anno: 2000,
pagine: 437 - 441
SICI:
0364-3190(200004)25:4<437:HINRLP>2.0.ZU;2-E
Fonte:
ISI
Lingua:
ENG
Soggetto:
PROTEIN-KINASE-C; RABBIT FOLLOWING STIMULATION; SYNAPTIC TRANSMISSION; LASTING POTENTIATION; PERFORANT PATH; DENTATE AREA; 2 COMPONENTS; PHOSPHORYLATION; GLUTAMATE; ACTIVATION;
Keywords:
hepatic encephalopathy; synaptic plasticity; glutamatergic system; learning; memory;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
28
Recensione:
Indirizzi per estratti:
Indirizzo: Munoz, MD Hosp Ramon y Cajal, Dept Invest, CSIC, Ctra Colmenar Km 9, E-28034 Madrid,Spain Hosp Ramon y Cajal Ctra Colmenar Km 9 Madrid Spain E-28034pain
Citazione:
M.D. Munoz et al., "Hyperammonemia impairs NMDA receptor-dependent long-term potentiation in the CA1 of rat hippocampus in vitro", NEUROCHEM R, 25(4), 2000, pp. 437-441

Abstract

Hyperammonemia is considered the main factor responsible for the neurological and cognitive alterations found in hepatic encephalopathy and in patients with congenital deficiencies of the urea cycle enzymes. The underlying mechanisms remain unclear. Chronic moderate hyperammonemia reduces nitric oxide-induced activation of soluble guanylate cyclase and glutamate-induced formation of cGMP. NMDA receptor-associated transduction pathways, includingactivation of soluble guanylate cyclase, are involved in the induction of long-term potentiation (LTP), a phenomenon that is considered to be the molecular basis for some forms of memory and learning. Using an animal model we show that chronic hyperammonemia significantly reduces the degree of long-term potentiation induced in the CA1 of hippocampus slices (200% increase in control and 50% increase in slices of hyperammonemic animals). Also, addition of 1 mM ammonia impaired the maintenance of non-decremental LTP. The LTP impairment could be involved in the intellectual impairment present in chronic hepatocerebral disorders associated with hyperammonemia.

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Documento generato il 02/04/20 alle ore 12:55:11