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Ammonia‐induced deficit in corticostriatal long‐term depression and its amelioration by zaprinast
Author(s) -
Chepkova Aisa N.,
Selbach Oliver,
Haas Helmut L.,
Sergeeva Olga A.
Publication year - 2012
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.2012.07806.x
Subject(s) - zaprinast , hyperammonemia , long term depression , glutamate receptor , neuroscience , metabotropic glutamate receptor , stimulation , pharmacology , medicine , chemistry , receptor , psychology , ampa receptor , guanylate cyclase
J. Neurochem. (2012) 122 , 545–556. Abstract Hyperammonemia is a major pathophysiological factor in encephalopathies associated with acute and chronic liver failure. On mouse brain slice preparations, we analyzed the effects of ammonia on the characteristics of corticostriatal long‐term depression (LTD) induced by electrical stimulation of cortical input or pharmacological activation of metabotropic glutamate receptors. Long exposure of neostriatal slices to ammonium chloride impaired the induction and/or expression of all studied forms of LTD. This impairment was reversed by the phosphodiesterase inhibitor zaprinast implying lowered cGMP signaling in LTD suppression. Polyphenols from green tea rescued short‐term corticostriatal plasticity, but failed to prevent the ammonia‐induced deficit of LTD. Zaprinast counteracts the ammonia‐induced impairment of long‐term corticostriatal plasticity and may thus improve fine motor skills and procedural learning in hepatic encephalopathy.