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Cellular mechanisms of the neurotoxicity caused by hyperammonemia and hypoglycemia

Posted on:1993-04-11Degree:Ph.DType:Dissertation
University:Dalhousie University (Canada)Candidate:Fan, PingFull Text:PDF
GTID:1474390014996034Subject:Animal physiology
Abstract/Summary:
Hyperammonemia and hypoglycemia are metabolic disorders which interfere with the function of the central nervous system. Cellular mechanisms of disturbed neuronal function in these two conditions were investigated in rat hippocampal slices with the use of extracellular and intracellular recording.;Low glucose concentrations (0.2-1 mM) seen in hypoglycemia caused mostly biphasic membrane potential changes: a small initial hyperpolarization followed by a large depolarization. Occasionally only one of these potential changes was observed. Input resistance of the neurons always decreased. Low glucose also interfered with synaptic transmission: first the generation of action potentials by EPSPs was inhibited, while later the size of EPSPs decreased. Quisqualate and NMDA currents were first potentiated, then inhibited.;Results suggest that NH;Synaptic transmission from Schaffer-collaterals to CA1 pyramidal neurons was diminished by as little as 0.5 mM NH...
Keywords/Search Tags:Cellular mechanisms, Synaptic transmission
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