Taurine protects against ammonia-induced impairment of hippocampal synaptic plasticity AN Chepkova, OA Sergeeva, HL Haas Institute of Neurophysiology, Heinrich-Heine University Hyperammonemia (HA) is thought to be responsible for alterations in cognitive functions in patients with liver failure and the congenital deficiencies of the urea cycle enzymes. Acute HA leads to cell damage via overactivation of glutamate NMDA receptors and hyperproduction of free radicals, while chronic HA results in an irreversible impairment of NMDA receptor function. Hippocampal long-term potentiation (LTP) is an NMDA receptordependent form of synaptic plasticity presumably involved in the mechanisms of learning and memory. With the objective to examine whether it is impaired by ammonia and if this impairment can be reversed by taurine, hippocampal slices from 812 week-old male C57BL16 mice were preincubated in either standard medium or in the medium containing 1 mM ammonium chloride, alone or in combination with 1 mM taurine or some other antioxidants and osmolytes. Significant impairment of LTP was found in the ammonia-preincubated slices: the mean increase in the CA1 field EPSP slope 60 min after high-frequency stimulation of Schaffer collaterals was 16.6I4.7% vs 32.2.I3.7% in the control (p<0.01). This deficit in hippocampal LTP was reversed by treatment with
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83rd Annual Meeting DPG. Abstracts pp S111-S133
Follow Pflügers Archiv European Journal of Physiologyl of Physiology
, Volume 447 (1)
Springer Journals – Mar 1, 2004
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