Glutamatergic neurotransmission in hepatic encephalopathy.
There is increasing evidence that glutamatergic neurotransmission is perturbed in hepatic encephalopathy (HE). Studies of the glutamate receptor system suggest that glutamate receptor density is reduced in different animal models of HE. Glutamate release and/or uptake is also believed to be altered in the disorder resulting in increased glutamate concentrations in the synaptic cleft. The relevance of these findings to the pathogenesis of HE remains to be clarified.
Maddison
J E
JE
Department of Pharmacology, University of Sydney, NSW, Australia.
Watson
W E
WE
Johnston
G A
GA
D000818:Animals; D001921:Brain / Q000503:physiopathology; D016291:Dizocilpine Maleate / Q000378:metabolism; D004285:Dogs; D018698:Glutamic Acid / Q000502:physiology*; D006501:Hepatic Encephalopathy / Q000209:etiology / Q000503:physiopathology*; D006801:Humans; D066298:In Vitro Techniques; D051381:Rats; D017470:Receptors, Glutamate / Q000502:physiology; D009435:Synaptic Transmission / Q000502:physiology*; D018350:alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid / Q000378:metabolism
D017470:Receptors, Glutamate; D018698:Glutamic Acid; D016291:Dizocilpine Maleate; D018350:alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid