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Glutamate and glutamine in brain disorders

Glutamate and Glutamine Homeostasis in Selected Brain Disorders. 199... [Pg.196]

Behavioral disorders such as anorexia, sleep disturbances, and pain insensitivity associated with hyperammonemia have been attributed to increased tryptophan transport across the blood-brain barrier and the accumulation of its metabolites. Two of the tryptophan-derived metabolites are serotonin and quinolinic acid (discussed later). The latter is an excitotoxin at the N-methyl-D-aspartate (NMDA) glutamate receptors. Thus, the mechanism of the ammonium-induced neurological abnormalities is multifactorial. Normally only small amounts of NH3 (i.e., NH4 ) are present in plasma, since NH3 is rapidly removed by reactions in tissues of glutamate dehydrogenase, glutamine synthase, and urea formation. [Pg.340]


See other pages where Glutamate and glutamine in brain disorders is mentioned: [Pg.195]    [Pg.199]    [Pg.201]    [Pg.203]    [Pg.205]    [Pg.207]    [Pg.209]    [Pg.211]    [Pg.195]    [Pg.199]    [Pg.201]    [Pg.203]    [Pg.205]    [Pg.207]    [Pg.209]    [Pg.211]    [Pg.204]    [Pg.402]    [Pg.103]    [Pg.276]    [Pg.508]    [Pg.199]    [Pg.207]    [Pg.62]    [Pg.681]    [Pg.718]    [Pg.228]    [Pg.944]    [Pg.266]    [Pg.340]    [Pg.97]   


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